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Behind the Knife ABSITE 2026 - Stomach · Behind The Knife: The Surgery Podcast

• 5 Stomach - Final Edits [00:00:00] Okay, behind the knife ab side review. The topic today is stomach. So Kevin let's start with some anatomy as always. So can you please walk us through, what's the blood supply to the stomach? Yeah, the, the stomach has some redundant blood supply. So there's quite a few vessels that feed it. We'll keep it simple to start here. You got your left gastric and you've got your right gastric. The left gastric is coming off the celiac artery and the right gastric is coming off. The proper hepatic artery, and that feeds the lesser curve of the stomach. And then for the greater curve of the stomach, you've got your gastroepiploic, both your right and left gastroepiploic. The right gastroepiploic is a continuation of the GDA. And the left gastroepiploic is coming off the splenic artery. And then, of course, you've got some of your short gastrics also coming off the splenic artery. So we talked about it briefly in the esophageal chapter, but for patients who undergo esophagectomy and have a gastroconduit, what's the most important blood vessel to supply that conduit? That's the [00:01:00] right gastroepiploic artery. Right, absolutely. So we have to preserve that right gastroepiploic. It's a very important vessel during esophagectomy. So there's some high yield classification systems when it comes to the stomach, and one of those is for hidal hernias. It's important clinically and it's important to know for the AB site. So, John, what are the different types of hidal hernia and how does that affect management? Yep. So there's four types of hidal hernias. You got type one through four. Type one is the most predominant, a greater than 90%. It's a sliding hernia. And how do we manage that? We typically do a repair only if it's symptomatic. The next type is type two, and that's a paraesophageal hernia. And typically we repair that. Type 3 is a sliding plus a parasophageal hernia. It also gets repaired when it's found. And finally type 4 is the entire stomach plus another organ, most commonly the colon is part of the hyal hernia and we also repair that if found. Yeah, absolutely. Yeah. So that type one, which is that G junction slides up above the diaphragm [00:02:00] And then the type two to four which is more of a true herniation of the actual stomach or other Contents up and those are at risk for bolivulus and a risk for incarceration and strangulation. So we absolutely need to repair those We'll have a good image in the ab site companion. So make sure you look at that and understand those different distinctions. So when we talk about malignancies there's the Siewert Stein classification for GE junction tumors. So, Kevin, what, what, what are those? Yeah, so it's type 1 through 3. Type 1 is a cancer in the distal esophagus, so 1 to 5 centimeters above the anatomic EG junction. Type 2 is in the cardia. So it's within one centimeter above and two centimeters below the EG junction. And then type three is subcardial stomach. So two to five centimeters below the EG junction. Yeah, so the way that might present on the outside is they may just tell you, you have a Seward Stein type two [00:03:00] tumor and ask you what type of resection you need to do for that tumor in that location. Just be aware of that classification system and that it's clinically used. So be sure to review that. John gastric ulcers. We're moving on with our classification systems for different pathologies of the stomach. What are the different types of gastric ulcers? Yeah, the gastric ulcer stuff is, is kind of difficult to understand because it's not intuitive, but there's type one through five. And type one is an ulcer located on the lesser curve. Type two is a ulcer on the lesser curve and the duodenum. So there's two ulcers there. Type three is a pre pyloric ulcer. Type four is an ulcer on the proximal lesser curve or the cardia of the stomach. And type five are diffuse ulcers that are usually caused by NSAIDs. So John, which of those type one through four are secondary to high acid production? So that'd be your type two and type three [00:04:00] ulcers. Great. Okay. So moving on to some pathology out of anatomy and classification systems. Let's talk about gastric body lists. Kevin how, how does gastric body list present? Yeah. So the classic presentation is the bore charts triad. So the epigastric pain retching and inability to pass an NG tube. Yeah, so, the way this will be asked on, on the test, and they'll give you somebody with a parasophageal hernia because they are associated with parasophageal hernias and they'll have that triad, that pain, retching, and the nurse is not going to be able to ask, or to pass an NG tube, and they're going to ask you what you want to do, and they, In that setting if you can't get them decompressed, the answer is, is going to be go into the operating room. John, what are the three, there's three different types of gastric volvulus. What, what are those? So you have organoaxial, which is the most common type of gastric volvulus, and that's a rotation along the axis of the stomach from the GE junction to the pylorus. And we'll have a good picture in to explain this within the text.[00:05:00] The next type is mesoaxial, which is less common. It's a rotation along the short axis of the stomach bisecting the lesser and greater curvature. And then finally you have the combined type where you have organoaxial and mesoaxial together. Yep, so yeah, make sure you review that image and have a good understanding of those different types. Kevin, how do we treat gastropodulus? Yeah, typically this is with emergent surgery, reduction, hernia repair, and gastropexy. Okay. And what if you have some strangulated stomach? Like what we mentioned before, fortunately the stomach is well vascularized, but let's say you have some dead stomach. Yeah, well then you're going to have to do a partial gastrectomy reconstruction. Okay. What if the patient is, are there any options, non operative options especially for patients who aren't good surgical candidates? Yeah, there's, there are endoscopic decompression ways that this can be treated. And how is that? So typically they do a gastropexy with double [00:06:00] peg tubes. Yeah, you need two points of fixation to prevent that stomach from rotating on itself. So, two peg tubes for fixation and gastropexy, but that's only in patients who absolutely will not tolerate a surgery. On the test, the answer is most likely going to be surgery. Unlikely to give you that sick of a patient that can't even undergo an operation. Jason, how would we approach a patient with gastroenvolvus clinically? Yeah, that's a good question. Well, first you need to, the basic principles of resuscitating the patient need to communicate with your anesthesia provider because they're a very high risk for aspiration during induction. If the patient could tolerate it, this, I would approach this patient minimally invasively as long as they would be able to tolerate the pneumoperitoneum. But from there you just, you reduce it like you would approach any, you know, peristalphageal hernia. So you reduce it, performing mediastinal dissection. You will typically, it impacts the, the stomach and, and repair your hiatus. So Kevin, moving on to gastroesophageal reflux disease or GERD. So [00:07:00] when a patient presents, what are the symptoms that are considered alarm symptoms? Yeah. So these can include things such as dysphagia, odynophagia, weight loss, anemia, and GI bleeding. Okay. And what's, why are those considered alarm symptoms? Because this, it could be something more severe than just GERD. We need to get an endoscopy to rule out malignancy. Yeah exactly. It's typically not stuff we have to deal with the surgeons. It's usually primary care, but that might show up there. So if you have a patient with those symptoms, you need to, the answer will be to get an EGD. What about medical management at GERD? So the most important thing is lifestyle modifications such as weight loss, elevate the head of the bed, and avoiding aggravating foods. And then of course the kind of mainstay medical treatment is with PPI therapy. Okay. Yeah. So, PPI's really, you know, change the management of GERD. They're very effective. If you have symptoms or symptoms through the PPI or persistent symptoms, those patients need an EGD. What are the indications, John, for a [00:08:00] to get sent to a surgeon? Yeah. Typically we see these patients come to our clinics because they fail medical management due to that, or they desire not to have prolonged or lifelong PPI's. And also if they have esophageal, extra esophageal manifestation such as asthma, hoarseness, cough, chest pain, and aspiration. Okay, and what, how do we typically work these patients up preoperatively? Yeah, hopefully they'll have this done before they show up, but the preoperative workup is start with a barium swallow. You can do an up, or an upper endoscopy, either one usually go hand in hand. Ambulatory pH testing and then finally esophageal manometry. To evaluate for an underlying motility disorder. Yeah, it's going to be some combination of that and it really depends on the individual patients. So barium swallow is good for looking for esophageal motility. It's going to be a poor man's esophageal motility. As, as well as evaluating for a hiatal hernia. Of course, an upper endoscopy to make sure there's no mucosal lesions or barits or [00:09:00] malignancy. We'll talk a little bit more about ambulatory pH testing, you know, I'll tell you that if you haven't if you have esophagitis or embarrassed on your on your EGD. You don't necessarily need that because you can definitely see the sequela of that GERD and that reflux. But certainly patients without hiatal hernias that can be part of the workup as well. Esophageal manometry, that's important if you're thinking about doing an anti reflux procedure with a wrap, that you want to make sure that they have normal. Underlying mortality. So some combination of those tests, that's good. Talking more about that ambulatory pH, there's a scoring system that we use. What is that? And how is it calculated? Yeah, that's the demisture score. So the, the, the criteria that go into the demisture score is the percent of total time of pH less than four. It's the percent upright time where pH is less than four, a percent supine time of pH less than four. It's a number of reflux episodes greater than five minutes. It's the [00:10:00] longest reflux episode in minutes. And then we kind of calculate that and then the Meester score of 14. 72 or greater is consistent with reflux. Yeah, that's, that's classically how it's calculated. And again, yeah, 14. 72 seems like an oddly specific number, but yeah, greater than that is consistent with reflux. Now there's other things that are being done. With ambulatory PH testing the, the Bravo probe and those type of things that are a little bit different, as well as some different impedance testing. But the D Mister is the, is the classic one to know. With regard to that, let's say that you have a patient who maybe had, you know, prior GI surgical history and, and You're worried that maybe they have bile reflux. What would, what kind of testing would you need to do for that patient? Yeah, we work them up with an impedance probe and then it also would change your management, the surgical management down the line. How so? Instead of doing a typical GERD operation, we would do a Roux en Y [00:11:00] reconstruction. Yeah, so let's say they had a Biliroth 2, they had some bile reflux, those patients would get reconstructed with Roux en Y anatomy, and you would need to do impedance testing to diagnose that. Okay, Kevin, back to you. So, we're trying to get these patients ready for anti reflex surgery. What are the key steps of an anti reflex surgery? Yeah, I, I've definitely seen this as a testable item before. So what you're really trying to do is you're trying to restore the normal anatomic position of the stomach and the GE junction with at least three centimeters of intra abdominal esophagus. And so if you have any hernia associated with this, this must be completely reduced, which requires mediastinal dissection to make sure there's adequate esophageal mobilization, and then any defect in the diaphragmatic crura must be adequately closed with permanent suture. Okay, yeah, those are the basic principles, so, yeah, you need to restore that normal anatomy, bring that stomach, bring that G junction down below [00:12:00] back into the abdomen, below the diaphragm. Again, three centimeters of intra abdominal esophagus, perform your high mediastinal dissection in order to achieve that. Repair your hiatal hernia, repair your your cruise with a permanent suture. Then when it comes to time to, for the, the fundiplication, the wrap. Talk to me a little bit about that. What do we need to do there? Yeah, so you have to have a complete mobilization of the fundus to help recreate that anti reflux valve with the funduplication. And so usually you have a two centimeter long quote unquote floppy funduplication performed over a large bougie, something like a 54 French. And then some people prefer to do a partial fund application. Yeah, there's, there's more evidence now that with a partial fund application, you may have less incidents of dysphagia but equal symptom control. So a lot of people are now going to these partial wraps, the posterior 270, the toupee really being the most common. There's a few other variations but certainly either a full 360 Nissen or a partial wrap are [00:13:00] acceptable. And it depends on a surgeon preference for the most part. So John, let's say you're in the OR and anesthesia says they're having trouble ventilating the patient. What are you worried about? Let's say this occurred while you're doing your mediastinal dissection. What are you worried about and what are your next steps? Yeah, so this is a commonly asked question. I've seen it a few times. So, I'd be worried about a capnithorax. And the way we would treat the capnithorax is that we usually had a violation of the pleura. So we would enlarge the tear within the pleura to avoid a tension capnithorax. Additional ways to drain that capillothorax going forward, once you kind of alleviated the concern for tension, is place a red rubber catheter with one end to the pleura, and the other end into the abdomen. This helps equalize the pressures between the two cavities. At the end of the procedure, you bring one end of the red rubber outside the abdomen, and place it to water seal, while the salvo from anesthesia side is administered. And finally, if you really ran into issues you can decompress the chest [00:14:00] intraoperatively. So be sure to prep your lower chest in during beginning operation. Yeah, so capnothorax, it can happen with a tear in the pleura, especially if you create kind of a one way valve where stuff's going into the chest and then it can't come back out. You know, another key point that we failed to mention I think is be sure you lower your pneumoperitoneum, so lower the pressure in your pneumoperitoneum, that can help. But really you're trying to equalize those pressures between, between the chest and the abdomen. And for the most part you can, you can ventilate through that. Rarely will you need some form of decompression with either, you know, a percutaneous angiocath into the chest, but you want to know, be sure that you, you prep that chest in. So you have that as an option intraoperatively. The other way this will often present to including what you've asked me is, is that the anesthesia, we'll start talking about high end title CO2. And this is specifically when you're doing your medial stenotisection decafnithorax. The other things you must consider during that part is hypoventilation. CO2 embolus and malignant hyperthermia all cause high end [00:15:00] title CO2s during your operation. Absolutely. Great points. So Kevin, let's say you finish the operation and you get a chest x ray and the nurse calls you concerned with that the radiologist called them and said there was a two centimeter pneumothorax. What do you think in there? Yeah, so once again, I'm thinking that this is likely a capnothorax and not a true pneumothorax and it should resolve. So I'd go check on the patient and check their vitals and put them on some supplemental oxygen. And as long as they're not overly symptomatic we can generally watch these. But if they do become symptomatic or it's enlarging, then we'd have to consider aspiration or thoracostomy too. Yeah, you certainly don't want to blow it off, but for the most part, like you said, these are capnothoraxes. They quickly resorb. Usually the patients are not symptomatic and it doesn't require much other than some supplemental O2, but absolutely need to check on the patient and confirm their stability. John, so let's say the, the surgery goes well the patient's recovering. How do you want to [00:16:00] manage them postoperatively? Yeah, there's a few key things you want to do. And if you've ever been an intern taking care of these patients on the floor. You probably remember this, but you want to schedule the anti emetics immediately post operatively and not just put them PRN but actually schedule them and you want to avoid, to help avoid all nausea and retching that may occur. You want a soft diet for a few weeks and you want to avoid food such as meat, raw vegetables, bread, and carbonated beverages for about four to six weeks. Okay. Let's say the patient comes back to see you a couple weeks later, they're complaining of some, some dysphagia or some difficulties swallowing. How do you want to manage that? Yeah, so if they can maintain hydration and still take oral intake, minor dysphagia can be typically managed expectantly, so you can wait it out. It's, it's a common occurrence after a wrap. A severe dysphagia, and especially if they're getting, you know, they can't tolerate any liquids, you want to get an esophagram and you're concerned for a technical error, such as a wrap is too tight. And if you have dysphagia persisting past [00:17:00] six weeks post operatively, You also want to get an esophagus, and is this is where you're concerned for a recurrent hernia or a slid a, a wrap that slid? And if that's not present, you also may want to consider dilation depending on what your anatomy looks like. Yeah. So almost all patients get some form of some mild dysphasia after a wrap. It generally resolves with time. So as you say, if it's severe and they can't handle their own secretions, well that's of technical error and that patient needs to go back to the or, but otherwise. You can kind of manage them and expectantly and if it's persistent you know, work it up and potentially perform a little dilation if there's not a, a technical air. Okay. So very similar, but with some nuances is the treatment and management of a hiatal hernia. So Kevin, how do we diagnose hiatal hernias? So often these can be seen on chest x ray but to kind of formally visualize it generally we get a CT scan. And then as we're working these patients up, they'll generally get a barium swallow and an EGD. Okay, yeah, great. So those are all ways that you can, that these are [00:18:00] diagnosed. So, John had previously mentioned it, but what's the management based on type of hiatal renal? Yeah, so for type 1 if they have, don't have significant reflux disease, you don't need to repair these. And if you do repair them, you use the same indications as for the GERD patients. And then for all symptomatic parasophageal hernias, types two through four, these should be repaired, especially if there's any obstructive symptoms. Yeah, so, so for what, even if they're hernias do all those require a repair? I think it's a patient dependent thing. If it's an elderly patient that, you know, is asymptomatic, you can maybe observe it. Yeah, I would say that for parasophageal hernias, they should be repaired on a routine basis in almost everybody. Now, if they're a very poor surgical candidate, you know, watchful waiting is an option, but Really all of these, if they can be repaired, should be repaired because they are a risk for, for long term volvulus. So laparoscopic repair is really the preferred approach when it [00:19:00] comes to the hiatal hernias. Although there are certainly open and even trans thoracic approaches for certain patients. Really the key steps is reduction of that hernia, so you need to mobilize and reduce that hernia sac. That's going to decrease your early recurrence. The use of mesh is somewhat controversial. For, you know, the guidelines and the data would support the use of an absorbable mesh for very large hiatal hernias over eight centimeters. Eight centimeters is kind of cut off, but really it's more if it's under tension or the tissues aren't that well. And you need some buttress of an absorbable mesh there. You can, you can put one in just understanding that that might increase your incidence of having postoperative dysphagia. And there is no evidence that long term that reduces a recurrence, but it may improve and reduce short term recurrences. There's, you know, insufficient evidence to really recommend one way over another of of, of, or one technique over another or the use or not use of mesh. But it is reasonable with those [00:20:00] large defects. And again, if those tissues are compromised in any way, need to be sure that you use a permanent suture when you perform your cruroplasty or close that crura. And then you're using a, performing a fundiplication any of the ones that we talked about previously at the time of the repair. Again, it's really kind of the same principles as your anti reflex procedure for GERD. So, John, let's say that we've performed our, we've reduced our hernia. We've done a high circumferential mediastinal dissection of the esophagus, but we just can't get that three centimeters of intra abdominal esophagus that, that we're shooting for. Do we have any options? Yeah, the first option would be to increase or further your mediastinal dissection to try to pull everything down. But your next option would be a colus gastroplasty. And this is an esophageal lengthening procedure that may be used if unable to obtain an adequate intra abdominal esophageal length. Yeah. Yeah. It's unlikely in reality, you would ever have to do that. [00:21:00] Normally, if you're performing your high mediastinal dissection, you can get adequate intra abdominal esophagus in almost all circumstances. But I have seen this show up on the test and that, and that's what you do. If, if you can't do that, and they, they give you the option. It's a cause gastroplasty. So, let's move on to Gastroduodenal Ulcer Disease or Peptic Ulcer Disease. So, Kevin, what's, what's the association with Peptic Ulcer Disease and, and h Pylori? Yeah, there's a very close association. So H. pylori is found in 75 percent of gastric ulcer disease and 95 percent of duodenal ulcers Yeah, that's exactly right. There's a high association, especially with those duodenal Ulcers, what's the treatment? So the classic triple therapy, which is a PPI chlorthomycin In amoxicillin or metronidazole. Yep, make sure you know that because they may ask you for those specific drugs in the treatment of H. pylori. So, John, what about stress ulcers, gastric stress ulcers? What are risk factors that set patients up for this? Yeah, these are [00:22:00] what we typically see in the ICU. So prolonged ventilation greater than 48 hours is one risk factor. Quagulopathy head trauma, also known as Cushing's ulcers. Burns, which are known as curling ulcers and obviously if you have a history of peptic ulcer disease, that's a high risk for gastric stress ulcers. Yeah, what are your high, what are the two most important factors? That would be your prolonged ventilation and coagulopathy. Yeah, those are the ones with the highest, I mean, we hear about the head trauma, the Cushing's ulcers, the, the burns, the curling ulcers, those are certainly risk factors, but the, the ones that are most strongly associated is that prolonged ventilation and coagulopathy. Kevin, what's the association with malignancy for both gastric and duodenal ulcers? Yeah, so the gastric ulcers have a higher risk of malignancy as compared to duodenal ulcers. So, biopsy is recommended for gastric ulcers, but not necessarily for duodenal ulcers. Yeah, most of those duodenal ulcers are that acid associated or H. pylori associated, but certainly gastric ulcers. [00:23:00] Still lower risk overall for four ish percent risk of malignancy associated, but you certainly want to buy up to those gastric ulcers. John, what's the management principles for, for when we're dealing with bleeding ulcers? So the first step like most people who are extremists is resuscitative measures. But the next step after that would be early endoscopy and NG2 placement to confirm, you know, where your bleeding is coming from. Rapid upper endoscopy is usually diagnostic and therapeutic. The way we can treat this bleeding not usually done from the surgeon's side is using endoscopic clips, thermal coagulation, injections of vasoactive or sclerosing agents. Yeah, exactly. So resuscitate endoscopic are, are very effective. So these, these interventions that you mentioned, the clips, the coagulation, the injection of the vasoactive sclerosing agent, those are typically 90 percent effective for the, to control initial bleeding. So what. Kevin, we talked about a patient's risk of re bleeding and there's a [00:24:00] classification. It's called the forest classification. So how, how does what you see endoscopically predict the chances of a re bleed in a patient with a bleeding ulcer? Yeah. So, we're gonna start with the lowest and go to the highest. So if you just see a clean base with no visible vessel or clot, it's a very low risk of re-bleeding less than 5%. If you see adherent clot, there's a 15 to 25% risk of bleeding of re-bleeding. If you actually see the vessel, then there's up to a 50% chance of re-bleeding. And then of course, if you have actively bleeding pul tile vessel, it's up to 80%. As it's actively bleeding. Great. And you'll see that sometimes on the outside, they'll, they'll describe those to you and they'll say, you know, which of these have the patients have the highest risk of re bleeding. So I would always mix up adherent clot and visible vessel. So it's actually visible vessels, higher risk. Yeah, that's what, that's the two they always give you is the adherent clod or the visible vessel. Yeah, and the visible vessel [00:25:00] is higher risk. Of course, the highest is a pulsatile bleeding vessel, but that one's kind of obvious. Okay, so moving on to gastric ulcers. Well, actually, before we do that, so let's, Let's say Kevin that you, you have a patient with a gastric bleed and they're successfully endoscopically managed, but then now they're in the ICU and they re bleed. What do you do in that situation? So generally... They should have another attempt at endoscopy. Yeah, absolutely. And that shows up on the test as well. If the patient does re bleed, the second attempt at endoscopy, as long as they're stable. If they're floridly unstable, you may have to go to the operating room. Alright, so what do we do in the operating room then? Yeah, okay, so let's go there. So for bleeding that cannot be controlled endoscopically or the patient is unstable in hemorrhagic shock, You, you take them to the operating room midline laparotomy, perform an anterior gastrotomy, and then over sew the bleeding area. Again, you want [00:26:00] to make sure you're biopsy, because these can be associated with a malignancy, and then you close your anterior gastrotomy. So let's keep moving on then from gastric ulcers now and talk a little bit about duodenal ulcers. So, Kevin, what's the management for a bleeding duodenal ulcer? So the initial management is the same as any upper GI bleed. You resuscitate, you put an NG tube down, and then you do a rapid EGD for diagnosis and treatment. Yep. Again, so endoscopy you're likely not going to know if it's a gastric or duodenal ulcer until you get in there. So the management is the same as, as bleeding gastric ulcers, you know, the difference of being that again, for duodenal ulcers, you know, the, there's no emphasis on biopsy like there is for gastric ulcers. The surgery is again reserved for uncontrolled bleeding or the hemodynamic instability. It's it's the first and second line of management is endoscopic management. But let's say that you do have to go to the operating room John, what's, what do you do for a uncontrolled hemodynamic, unstable [00:27:00] patient with a bleeding duodenal ulcer? So the classic operation is a longitudinal anterior duodenotomy at the duodenal bulb and the incision can be carried across the pylorus if necessary. We want to control the bleeding with three point U stitch technique. So, sutures are placed superior and inferior to the ulcer to control the bleeding from the main vessel. And we want to make sure we take care to avoid the common bowel duct. A medial stitch is also then placed to control the black backbeating from the transverse pancreatic artery. We can also ligate the GDA above the duodenum if we're unable to control the bleeding with the U stitch. And finally, we want to perform a transverse duodenotomy closure. And you should also be aware that there are therapeutic angiographic interventions that can be done, and it's somewhat institution specific as to where that falls in the algorithm but those are becoming more popular, so be aware of those. There are certainly downsides, like ischemia to the duodenum but for, you know, for the test the, the, the answer is most likely going to be [00:28:00] endoscopic. And then if they're unstable and you can't control it, go to the OR. Now Kevin how do we treat we talk about bleeding ulcers, what about perforated ulcers? What are some management principles for those? Yeah, so these patients present pretty sick many times. And so you're going to start with resuscitation and NGD compression, and a high dose PPI, and antibiotics for empiric coverage of gram naked rods, oral flora, and anaerobes. And then sometimes you'll consider adding antifungals in the high risk population. But generally, you need to get these patients to the operating room for a mental patch repair. And what is that? What's a Nomental Patch Repair? So, you can do this open or laparoscopically. But generally you, you know, identify the perforation and you take some, you know, after irrigation and cleaning it up you put a well perfused omentum over the perforation site secured with three or four sutures. Yeah, okay. Yeah, that's our gram patch. There's a couple variations on it. We can attempt closure of the perforation if able to approximate the edges, but usually the tissues are not well and [00:29:00] in your classic description of the gram patch there was no closure of the perforation, but some people do do that. You need to be sure that you leave a drain. And John, what about really large perforations? Like, let's say there's a big three centimeter duodenal perforation how can you, what are your options there? Yeah, so these ones can be very difficult to deal with and a grand patch typically won't work in these situations. So we could consider doing a jejunal serosal patch, also known as a thou patch. So John, you know, sometimes we hear about doing an acid reducing procedure at the time of a surgery for a perforated ulcer. So let's say the patient is undergoing the operation for a complicated gastrointestinal ulcer and they have a long history of being on PPIs and they've had H. pylori and they've had it Documented that it's been eradicated. So in other words, they have, you know, medically or they have refractory ulcer disease. What do you think about these acid reducing [00:30:00] procedures? What are they? So the classic the most common or classic one is the truncal vicotomy. and pyloroplasty. However, nowadays, we will typically perform a highly selective vagotomy, which then preserves the motor innervation to the pylorus, eliminating the need for a drainage procedure. Your final option is a vagotomy and an entrectomy. These have higher morbidity, just due to the need for a Bellroth reconstruction. But they are reserved for patients that are stable and have anatomic indications such as a large antral ulcer or pyloric scarring. Yeah, we're certainly doing less and less of these as PPI's are very effective, but you know, if they give you that scenario where they're laying all that out for you, that they've been treated for everything and they still got this, you would want to consider doing one of these acid reducing procedures. That's where they're trying to lead you. I should mention just briefly that, you know, marginal ulcers after bariatric surgery are, it's a very similar presentation and they're managed exactly the same as a duodenal ulcer. So let's move on now [00:31:00] to some gastric neoplasms. So let's start with hyperplastic polyps. Kevin, what are hyperplastic polyps and what do you do about them? So these are the most common polyps and they have a very low malignant potential. If they're under half a centimeter, you can observe them. If they're greater than half a centimeter, you need to do endoscopic resection and biopsy of the surrounding mucosa. Okay, great. Moving on to another very common neoplasm in the stomach is a gastrointestinal stromal tumor. So what are those and what is their malignant potential? So this is the most common mesenchymal tumor of the GI tract. They have malignant potential as is based on the size and number of mitoses per high powered field. Great. So these just, you know, these originate from those interstitial cells of Kajal. You may see that on there. Their, their pathology will show either spindle or epithelial cells. These are generally CD117 or CKIT gene positive. Other things you might see on your pathology report or in the [00:32:00] question stem is CD34, DOG1. Desmond Menton. And other are, those are all other possible markers. There's a, a variation called the P-D-G-F-R-A that's an alternate oncogenic pathway. So unfortunately you do need to memorize these 'cause these might show up in a question stem and, and that might be your only clue to identify that you're dealing with a, a gist. You know, it's important to note that a gist metastasized through, homogenous spread. They don't go to lymph nodes. Most common a distant mat is to the liver into the peritoneal surfaces. So, you know, there, there is a, a staging of just, and that's in the, the abscite companion for you to review. But really the important things are the things that portend a poor prognosis. So what are those factors that that lead to a poor prognosis for patients, John? Yeah. So that's if you have a gist let's look in the esophagus, colon or rectum, they have poor prognosis. If it's [00:33:00] large, greater than 10 centimeters, and if it has 10 mitoses per 10 high power fields. And loca local evasion to surrounding structures or distant metastases are all po poor prognosis factors. Yeah, that's great. So again, location, esophagus, colon, rectum. They're large size 10 centimeters high mitotic rates, 10 mitosis per 10 high per field. Local invasion and distant mes are, are, are your poor prognostic factors? Kevin, treatment of a gist? Yeah, so this is an in block surgical resection with a one centimeter margin. Okay, what about when would you consider neoadjuvant therapy and what is a neoadjuvant therapy? Yeah, so you can use a neoadjuvant Mantinib or Gleevec for large and locally advanced tumors. Okay, yeah a little bit vague there, but yeah, large, again, those poor prognostic factors you can consider adding neoadjuvant Gleevec. Again, we talked about you, you're right in block resection, one centimeter margins. There's no need for a lymphadenectomy. 'cause again, these don't spread, typically spread to lymph nodes. [00:34:00] So resection of, of the primary tumor is even considered and often indicated even in metastatic disease for palliation for symptom control. Sometimes these can bleed, sometimes they can obstruct. And then adjuvant imatinib when do you add that? For those at intermediate or high risk of recurrence based on tumor biology. Yeah, you know, the cutoff used to be 5 centimeters and greater than 5 mitoses per 5 high powered fields. It's a little bit more, the, the, the, it's, the indication has been expanded. So it's more of those patients that are deemed to be intermediate or high risk. Again, that's somewhat vague. But just be aware that imatinib is an option for both neoadjuvant and adjuvant setting to lower that risk of recurrence or spread. So what we're talking a lot about this Gleevec imatinib. Kevin, what is that? Yeah, it's actually a tyrosine kinase inhibitor. Yeah, exactly. So, there are going to be tumor tumors that are [00:35:00] resistant to, to Gleevec based on their oncogenes. And so what's an option for a imatinib resistant gist? Yeah. So they have a new drug now called sunitinib and it's actually a multi targeted receptor tyrosine kinase inhibitor. Okay. So moving on now to gastric cancer. So Kevin, what are risk factors for gastric cancer? Yeah, so you have H. pylori, smoking, heavy alcohol intake, high salts and nitrates. Yep, okay, great. So these are typically classified as intestinal type or diffuse type. That's the Loring classification. Most are sporadic. There's 5 10 percent that are familial. And three to five percent of that are associated with an inherited syndrome such as a hereditary diffuse gastric cancer, which is an autosomal dominant disorder that is secondary to germline mutations in the CDH1. Believe it or not, I have seen that on the exam before, that CDH1 association with hereditary diffuse gastric cancer. How do you treat these patients? These patients with this [00:36:00] hereditary diffuse gastric cancer, again, CDH1, just burn that into your memory. Yeah, it's a terrible problem and they need to get a prophylactic gastrectomy generally between the ages of 18 and 40. Yep the prophylactic gastrectomy sounds extreme but that's for those CDH1 carriers. Women with CDH1 are at increased risk of breast cancer as well, similar to BRCA patients. So also remember that association. John, what are some other hereditary syndromes with an increased gastric cancer risk? Yeah, some ones that you might see pop up is Lynch syndrome, which is a DNA mismatch gene. Juvenile Polyposis Syndrome, which is your SMAD4 gene Pute Jager Syndrome, and then finally Familial Automotivus Polyposis, which is your APC gene on 5q21. Yeah, great. So, you know, these, these gene associations, they're, they're terrible, they're annoying, but sometimes, occasionally, they will show up on the exam. So they're worth reviewing to get those easy points. So Kevin, you have a patient that has a gastric cancer. So how do you go about [00:37:00] staging gastric cancers? Yeah, for these patients you get routine labs and then what's critical to it is your CT chest, abdomen, and pelvis. And then you need to do your endoscopic ultrasound with FNA and generally a PET scan also. Okay, great. Yeah. Labs, CT chest, abdomen, pelvic, EUS, FNA and a PET CT for gastric cancer. What about the role of a staging laparoscopy John? So, the NCCN recommends laparoscopic staging with peritoneal washings for clinical stage greater than T1B tumors if chemoradiation or surgery is being considered. It's not needed if known metastases or if they're undergoing definitive chemoeration or palliative options. Right. Okay. Yeah. So if they're, if they're, you know, going to get neoadjuvant or they're undergoing definitive chemo rads palliative options obviously don't need a staging laparoscopy, but yeah, greater than T1B tumors will need a staging laparoscopy according to MCCN recommendations. Okay, we're gonna go through some staging [00:38:00] pearls. Fortunately, a gastric cancer staging is very similar to esophageal cancer with the addition of the cirr rosa. So for your T stage, your your T one A invades the lamina propria or the muscularis mucosa, whereas T one B invades the submucosa. Again, that's that distinction between T one A and T one B for the need for a staging laparoscopy. T one B invades submucosa. T2 invades the muscularis propria, where T3 invades the subsorosa, and T4 invades through the sorosa into adjacent structures. For your N staging, so N1 is one to two nodes, N2 is three to six, and N3 involves seven or more nodes. And then, of course, M0 and M1 is either the presence or absence of distant metastasis. So again, very similar to esophageal cancer, but the esophagus does not have that sclerosis. So, Kevin, what is considered unresectable disease in terms of gastric cancer? Yeah, so this is when you have [00:39:00] peritoneal involvement or distal metastases. Also, if the root of the mesentery is involved or there are any para aortic nodal disease confirmed by biopsy. And then, of course, any encasement of major vascular structures also. Yeah, encasement of major vascular structures excluding the splenic vessels because you can do a splenectomy with your gastrectomy, so, but certainly encasement of any other major vascular structure would be unresectable disease. And again, peritoneal involvement, that's why that staging laparoscopy recommendation is there because that's considered unresectable. So John, what about neoadjuvant therapy? Who gets neoadjuvant therapy? Yeah, you see, these are patients with clinical T2 or higher. Any nodal involvement patients typically received the entire chemotherapy regimen upfront prior to surgery. And once again, this is similar to both esophageal and rectal cancer. Yep. Great. So yeah, the upfront therapy, that the complete upfront neoadjuvant therapy as you say, similar to esophageal and rectal cancer. So surgical principles. So let's say that they have resectable [00:40:00] disease and you're going to perform your gastrectomy. What, what are some surgical principles, Kevin? Yeah, so you want to have a resection with at least 6 cm margins and lymph node harvest of at least 16 nodes for staging, ideally close to 30. Yeah, so the type of resection either is a total versus subtotal gastrectomy, as well as the extent of lymph node dissection, D one versus D two, which we'll talk about here in a minute. It is somewhat controversial. Subtotal gastrectomy is preferred for distal lesions. So that sewer three, again, review those sewer classifications. For your partial gastrectomy you want to like, like Kevin said, a six centimeter proximal margin. The distal margin should be post pyloric with at least a 2cm margin, so 6cm proximal, passive pylorus 2cm. So proximal tumors, those SEWRT2 tumors will generally need a total gastrectomy with esophageal jejunostomy. The distal portion of the esophagus may need to be resected for adequate margins. [00:41:00] And tumors that are crossing that GE junction are classified and treated as esophageal cancer. So, John, what about the role of prophylactic splenectomy during your gastrectomy for gastric cancer? So you don't need to perform a prophylactic splenectomy. The only reason you would do this If the spleen or the hilum were grossly involved with the tumor. Yep, we talked about if there's that does not make it unresectable if it's, if it's associated with those splenic vessels. Kevin I mentioned a D1 versus a T, D2 lymph node dissection. What are the types of lymph node dissections with gastric cancer? Yeah, I think the most important ones to know are the D1 and the D2. The D1 is where you take the perigastric nodes along the greater and lesser curve. So it's generally always done in these stomach cancer cases. Now, the D2 is the next level. It's basically where you trace out all the major vessels, the left gastric, the common splenic arteries, and you take the nodes along those vessels, and that's a more extensive dissection, has some more [00:42:00] morbidity associated with it. Then you can also get into further ones such as the D3. which is where you're going along the patadudenal ligament, the retro pancreatic space, the root of the SMV and the SMA. And then there's even a D4, which is where you get the periaortic nodes. Great. That's, yeah, that's a great way of breaking that down. It can be very confusing. So gastrocnemius with a D2 dissection. That, that's the standard in Asia. However, Western studies have failed to demonstrate survival between a D2 and a D1 dissection. And the D two dissection may be associated with increased morbidity or mortality. Although, you know, in those studies, the increased morbidity was likely attributed to the splenectomy, so there have been subsequent meta-analysis that showed AD two without splenectomy had superior re recurrence free survival and trend and trended to improved overall survival. The current NCCN recommendation is for an R zero resection with at least. D1 or modified D2 lymph node dissection. So Kevin, [00:43:00] when is adjuvant therapy recommended and what is it? Yeah. So if you have node positive disease or T3 or T4 tumor then you need to do adjuvant therapy. And generally it's adjuvant five for a year or so. Great. Okay. So let's move. Gastric cancer is a big topic. A lot of stuff to remember there, but it's certainly highly testable. So, make sure you review that several times. So let's move on to some post gastrectomy syndromes. So John, what's a, what are we, what's a retained antrum syndrome? Yeah, so that's retained anterior tissue within the duodenal stump after a gastric dissection. Yeah, so the G cells are then bathed in your alkaline fluid, and that leads to a continuous gasprin release, acid production in the proximal stomach remnant, and it can lead to ulceration. So you don't want to forget about those gastrin secreting tumors and, and those rare things. So, and just assume that it's retained antrum syndrome. So you do want to check gastrin levels to rule out a gastrin secreting tumor. But the treatment for retained antrum syndrome is PPI [00:44:00] as well as vagotomy and resection of that retained antrum. John, what about dumping syndrome? What's dumping syndrome? Yeah. So that's categorized as tachycardia, diaphoresis, and dizziness and flushing. There's two types. You have early dumping syndrome, which usually occurs between 20 and 30 minutes after a meal. And this occurs due to the abrupt hyperosmolar load to the small intestine. Then you have late dumping syndrome, which occurs 1 to 4 hours after a meal. And this is due to the rapid carbohydrate load to the small intestine resulting in a large insulin surge and rebound hypoglycemia. Okay, how do you manage I agree early, late dumping syndrome. How do you, how do you manage these? Yeah, it's usually dietary management. You can typically counsel a patient to do small meals and no sugary drinks to reduce that carbohydrate load. And then, but for refractory dumping syndrome, you can try octreotide. Okay, perfect. Now, we talked a little bit about bile reflux or alkaline reflux gastritis previously, but let's review it again. So what is [00:45:00] alkaline reflux gastritis and when does it occur? Yeah, it usually occurs after Bo Roth 1 and Bo Roth 2 reconstructions. The diagnosis, like we talked about before with impedance studies. The medical management that you want to use prokinetic agents and bio acid binding residents. And then you're kind of your ultimate surgical management would be a conversion to a Roux en Y. Okay. And what's an, what's an important principle when you, that conversion to a Roux en Y for bile reflux gastritis after a bilirubin 2 what's a key principle there? Yeah. You want to worry about your Roux limb length and you want to be at least 50 centimeters to avoid recurrent bile reflux. Okay. Great. Kevin, moving on. What about afferent limb syndrome? What is that? Yeah. So that's when you have an acute or chronic obstruction of the afferent jejunal limb following a Biliroth II reconstruction. And the, so yeah, that results in increased luminal pressure of that afferent limb. And what are the symptoms of afferent limb syndrome? So I just want to pause real quick here [00:46:00] because I found this slightly confusing when I was a trainee in what is the afferent limb. So it's also, you could also call it the biliopancreatic limb. So no food is passing through this. This is just where your bile and pancreatic enzymes are passing through as they meet up later. So what you can get with this is you can get acute or chronic obstruction and you can get obstructive jaundice, cholangitis, pancreatitis from back up pressure in the biliopancreatic limb. And then you can also get terrible things such as a duodenal stump blowout. And then occasionally you can get bacterial overgrowth in the afferent limb. Okay. What happens with that? What's, what's the mechanism behind that bacterial overgrowth in that afferent limb? What happens? Yeah, so the deconjugated bile acids result in steatorrhea, malnutrition, and vitamin B12 deficiency, leading to megaloblastic anemia. Awesome. So what is the treatment then? So you can start with treating these patients with antibiotics, so there's a high relapse rate. And so if you, if you need something further, you can convert this Biliroth 2 into either a Roux en Y with a long limb, or you can do a [00:47:00] Biliroth 1. Great. And it's also important to mention that if you, you get these patients, these Bill Roth II patients that present with a bowel obstruction, you know, you need to treat them like you would a patient with a similar to a Roux en Y anatomy is that you can't really decompress that afferent limb with NG decompression. So you need to take those patients to the operating room. Okay. Well, I think we've made it where we're moving on now to our quick hits for stomach. So, let's do it guys. Okay. Kevin. Thank you. Thank you. What are the lab findings seen with gastroparesis or gastric outlet? Obstruction. So generally they're gonna have a hypokalemic, hypochloremic metabolic alkalosis with elevated gastric levels. Yep, exactly. And the gastro is released is a, is due to the distension of the stomach. Okay. John, what do you do if you need more esophageal length doing during a paraesophageal hernia repair? We talked about it before. Yep. That would be a call gastroplasty. Call gastroplasty. Exactly. Okay, Kevin. You have a patient who is unable to swallow and handle their own [00:48:00] secretions after a NISN. What's the problem and what's the management? Yeah, so it sounds like the wrap is too tight. You need to return to the operating room and revise it. Exactly, you know, like we mentioned a little bit of dysphagia is to be expected But if they can't handle their own secretions that wraps too tight, you gotta go back to the OR. John, type of ulcers associated with increased acid output. That'd be your type 2 and 3. Yep, type 2 and 3 are associated with high acid output. Kevin, which ulcers are associated with decreased mucosal protection? Type 1 and 4. Yep, 1 and 4, decreased mucosal protection. Type 2 and 3, high acid output. John, you have a hiatal hernia that's discovered at the time of sleeve gastrectomy. What do you do? You want to repair the hiatal hernia. Yep, yep. So if you see an incidental hiatal hernia during a sleeve, the answer is repair it. Kevin, you have a patient with a history of antrectomy. He's got Biliroth 2 reconstruction. This was done in the distant past who presents with intermittent abdominal pain and distention, which is [00:49:00] relieved after a bilious emesis. He's got megaloplastic anemia on his laboratory workup. What is this? Yeah, this is a classic afferent limb syndrome, which we just talked about. So afferent limb syndrome. Okay. John, what's the diagnosis of a patient who has multiple duodenal ulcers and the gastrin level is over a thousand. That would be Zollinger Ellison syndrome. Exactly. And so, the gastrin over a thousand is diagnostic Zollinger Ellison syndrome. Kevin. So, there's a branch of the posterior vagus nerve that is missed during a highly selective agonomy. and results in recurrent ulcer disease. What is that nerve? This is the criminal nerve of GROSSI. An old criminal nerve of GROSSI, gotta make sure you get that. Okay John, so there's a gist mutation that is resistant to imatinib. Yeah. Yeah, that's the mutation. P-D-G-F-R-A. Yep. P-D-G-F-R-A. That would be a dirty question if they give you that and they ask you what the, the adjuvant therapy is, but [00:50:00] the P-D-G-F-R-A is resistant to Imatinib. Okay. Kevin a gastric mass with biopsy showing expansion of the marginal zone apartment with development of sheets of neoplastic, small lymphoid cells. What is the, so you see that in the test description, right? Marginal zone compartment, development sheets of neoplastic small lymphoid cells. What is the diagnosis and what is the treatment? Yeah, this is a maltoma and you can actually treat this with antibiotics. So the triple therapy for H. pylori will treat this. Yep, no surgery antibiotics. And, and that's the way they'll, they'll write it. They'll say, what is the treatment? And the answer is antibiotics. And Jason, let me throw one at you. What if you did have that resistance in that nib? What would you give them? As you mentioned previously, that's that Sunit nib. And that does it. That was a long one, but that's your stomach review for the Abcite. So thanks for listening.