Understanding Bariatric Surgery: Procedures, Outcomes, and Care
This podcast delves into the fundamentals of bariatric surgery, exploring four major procedures—gastric band, sleeve gastrectomy, Roux-en-Y gastric bypass, and duodenal switch. Learn about patient considerations, surgical impacts, and the importance of postoperative care for long-term success. Transcript [00:00] Hello and welcome back once again to Surgery 101, the podcast series brought to you with the help of the Department of Surgery at the University of Alberta. This is Jonathan White broadcasting to you [00:20] live from the Royal Alexandra Hospital in Edmonton, Alberta. This week’s episode is number 3 in a series on bariatric surgery and obesity, brought to us by medical student Julie La, who is visiting on a surgical educational active from McMaster University. In this episode, Julie will be getting to the main topic, the bariatric surgery [00:40] itself she’ll be giving a brief overview of the four main procedures, the gastric band, the gastric bypass, the sleeve gastrectomy and the juillenal switch. So let’s get ready to get all the way up into bariatric surgery itself here on surgery 101. [01:00] Hi everyone, my name is Julie Law and I’m a third and final year medical agent. [01:20] Student at McMaster University in Hamilton, Ontario. This podcast was written and produced with guidance and support from Jenny Marshall, program assistant in digital education, and Dr. Jonathan White, general surgeon at the University of Alberta, creator of Surgery 101. The expert content reviewers were Dr. Alia Kanji, bariatric surgeon at the University of Alberta, and Dr. Renika Moti, [01:40] assistant clinical professor in the Department of Family Medicine at the University of Alberta, and medical lead for the Edmonton Adult Bariatric Clinic. The topic of today’s podcast is surgical options for the management of obesity. By the end of this episode, you should be able to describe various types of bariatric surgery, including the adjustable gastric band, [02:00] sleeve gastrectomy, row and wide gastric bypass, and the duodenal switch. Let’s start by reviewing the NIH [02:20] guidelines for bariatric surgery. 1. Age 18 to 64 2. BMI greater than 40 or BMI greater than 35 with comorbidities such as type 2 diabetes, cardiovascular heart disease, severe obstructive sleep apnea, or GERD. 3. Some contraindications include current [02:40] substance dependency, recent major cancer, untreated psychiatric illness, diseases that would make you ineligible for any surgery, if you are pregnant, have cirrhosis, or chronic pancreatitis. Most bariatric surgery is performed by general surgeons with subspecialty training in minimally invasive surgery and bariatrics. [03:00] Bariatric surgery has been evolving since the 1950s. Many groups around the world recognized obesity as a medical issue and began to try various ways to reduce the size of the stomach, the concept of restrictive surgery, rearrange the intestines to facilitate malabsorption, and then eventually a combination of both. As we learn more about [03:20] how and why bariatric surgery works, we are learning that there are a number of gut hormones that are involved in augmenting weight loss in these procedures. These procedures, while initially done open, are now almost exclusively performed laparoscopically. In Canada, bariatric surgery is covered by our Public Health Plan, which is decided upon provincially. [03:40] With that, there is variation in procedures that are covered. In Ontario, where I’m from, the Ministry of Health funds three types of bariatric surgery, all of which are done laparoscopically. The Roux-en-Y gastric bypass, the vertical sleeve gastrectomy, and the duodenal switch. In Alberta, the duodenal switch is not yet performed, but the adjustable gastric bandage. [04:00] is. Now to review the steps in anatomy of bariatric surgery. These can be tricky to follow. Honestly, reading them in textbooks repeatedly was even difficult to follow. I hope that I’ve simplified things and the slides that we provided will be a helpful tool. This might be a section that needs a few listens. [04:20] The first procedure I’ll discuss is the adjustable gastric band. The gastric band was initially approved by the FDA in 2000. Since then, hundreds of thousands of these bands were placed around the world. The principle behind this procedure is the placement of a foreign body, the adjustable gastric band around the proximal [04:40] stomach. This is then connected via tubing to a port that sits on the fascia below the skin. The port can then be accessed to inflate the band with saline or deflate the band removing saline. The adjustment is to allow for more or less restriction. The band was initially a very attractive weight loss procedure as it is minimally invasive, adjustable, and [05:00] completely reversible. Unfortunately with it were many complications that led to a large number of these bands being removed. Next the components of the Roux-en-Y gastric bypass. This procedure includes the pouch, [05:20] which is a small segment of the stomach that is stapled off. It acts as the new gastric reservoir with a much smaller volume. This will help decrease overall intake and increase the sense of satiety or fullness. Next is the bypass part, where a distal portion of the small intestine, the jejunum, is divided and then attached to the gastric pressure. [05:40] pouch. This is called a gastrostomach to jejunum jejunostomy. This is the new pathway that food will travel and it’s called the Roo Lim. Recall the physiology of obesity. One simple way to look at it is energy in versus energy out. Using a distal portion of the small intestine will [06:00] result in bypassing a large absorptial surface, decreasing the amount of energy in. Okay, now about 100 to 150 cm downstream from this new connection, the proximal aspect of the jejunum from your division is connected to a downstream part of your small intestine. Remember, this connection goes [06:20] from the bottom part of your stomach, the distal stomach, from where the pouch was stapled off, all the way down to the proximal jejunum. But as you might notice, there’s an important area stuck between the stomach and the jejunum, the duodenum.
Understanding Artemisinin Resistance: A Conversation with Dr. Charlie Woodrow
Dr. Charlie Woodrow discusses the critical challenges of artemisinin resistance, its impact on malaria treatment, and the advancements in research that aim to combat this global health issue. Transcript [00:00:00] Interviewer: This is a podcast of the Nuffield Department of Medicine. Today we speak with Dr. Charlie Woodrow about his research on artemisinin resistance. Why is artemisinin resistance a problem? [0:00:10] Dr. Charlie Woodrow: I think artemisinins are a one-off drug. They are the most effective, most rapidly acting anti-malarial that we have and they’re very safe and well tolerated. So losing them is a major problem. Artemisinins are used in all anti-malarial treatments for the main form of malaria that we see around the world, falciparum malaria, and they’re used in combination with a partner drug. But all treatments should contain an artemisinin. So once we start to lose that activity, which is what we see in resistance, we have major problems both in treating individual patients and in controlling malaria as a public health problem. [0:00:49] Interviewer: And how has artemisinin resistance developed? [0:00:52] Dr. Charlie Woodrow: So that’s a classic example of evolution. So when you treat a patient with malaria and you do not kill all the the parasites, the survivors are more likely to be resistant to artemisinin. And the reasons why that might happen relate to why treatment might fail. So, patients who don’t complete their courses, patients who just take an artemisinin without this partner drug that we need as well, and there’s also a problem with fake or substandard anti-malarials which don’t contain enough of the compound. [0:01:25] The other big factor is the immune system. So we tend to see artemisinin resistance appearing in areas where patients have low immunity, what we would call low transmission settings. So that’s outside Africa. Resistance has generally tended to appear in Southeast Asia or South America. And for artemisinins, it has been Southeast Asia because the drug has been made in China for much of its lifespan. And so, the local availability of artemisinins has been high. And so eventually, because of evolution, we see resistance developing. [0:02:00] Interviewer: How can we counter these resistance strains? [0:02:02] Dr. Charlie Woodrow: So the simple thing is to give treatments correctly. So these artemisinin combination therapies to make sure that when we’re giving them, patients are completing the courses and that their infections are being cured. We can choose the partner drug that is used in combination with the artemisinin carefully to make sure that there is still efficacy for the partner drug and that’s more slower acting anti-malarials like Mefloquine or Lumefantrine. And then in the future we have to think about other alternatives. So, when we look at infections like HIV and TB, we would always treat those with three drugs and that’s a possibility for the future of malaria, although difficult to achieve in reality. [0:02:46] And beyond that, new drugs, but there are very few available at the moment. [0:02:53] Interviewer: What are the most important areas of research that have developed in the last five to ten years? [0:02:58] Dr. Charlie Woodrow: So I think the main area of research in this field has been the documentation of artemisinin resistance in the field. There was theoretical discussion about this before, but it’s quite clear that there is artemisinin resistance in the ring stage of the parasite. That’s a certain subset of the life cycle and that that’s developed across a wide area of Southeast Asia. [0:03:21] And then more importantly, in the last couple of years, we’ve understood this form of resistance and we’re beginning to understand in biological detail what the mechanism is and that’s important for several reasons. I think the first one is just to convince everybody that it’s a major problem. [0:03:40] If you can say this mutation in a particular gene happens with artemisinin resistance, then it’s much easier than the more conceptual idea that the parasites don’t respond so well in people. [0:03:54] And then understanding the mechanism, which in simple terms is a mutation in a particular protein which is called the Kelch 13 protein then allows us to study where resistance has spread to using quite simple techniques. [0:04:12] Interviewer: Why does your line of research matter? Why should we put money into it? [0:04:15] Dr. Charlie Woodrow: Understanding artemisinin and resistance both in terms of how far it’s spread across Southeast Asia at the moment and what the mechanism is, is fundamental to understanding how to treat patients, how to treat populations and how to eliminate malaria, which is a new goal that has been promoted by funding bodies and governments across the region. [0:04:40] So I think the main issue is how do we manage malaria over the next 20 to 30 years. If we don’t understand why parasites respond well or poorly to artemisinins, that’s going to be very hard. [0:04:54] Interviewer: And finally, how does your research fit into translational medicine within the department? [0:05:00] Dr. Charlie Woodrow: So I think continuing on that idea of elimination, I think this is the new goal for control of malaria in Southeast Asia. And having the means to be able to look at how artemisinins are operating in remote areas, I think is the biggest advance in the last year. So, we can take some blood that has been stored on a piece of paper, bring it to a central lab and using fairly simple forensic techniques, which is the polymerase chain reaction, PCR, we can actually determine whether parasites from rather remote areas, for example in Myanmar, which are very difficult to access with normal clinical studies, are resistant to artemisinins. [0:05:45] So I think that’s having a big effect in terms of control programs, in choosing how they treat malaria. And we’re also seeing lots of effects in terms of how people do science. So, we work with students and researchers from areas in Myanmar and other emerging
Eye Health Spotlight Tackling Glaucoma with Modern Care
This episode dives into glaucoma, focusing on its types, symptoms, and management. Learn about open-angle glaucoma, acute angle closure glaucoma, and surgical and medical treatments to prevent vision loss. Transcript 00:00] Hello and welcome back to Surgery 101. The podcast brought to you with the help of the Department of Surgery at the University of Alberta. My name is Jonathan White and I’m a surgeon here at the Royal Alex [00:20] Sandra Hospital in Edmonton. This week’s episode is the second in a series of five episodes all about the eye, brought to us by medical student Kim Papp. Last week we covered the basic structure and function of the eye. This week we get to feast our eyes on the topic of blood coma. We’ll be looking at the [00:40] of the condition, the different sorts that there are and the different treatment options. So let’s get ready to think about what happens when you’ve got a little bit too much pressure in your eye here on surgery 101. [01:00] Glaucoma. Welcome to this episode of Surgery 101 on glaucoma, where we will learn the basics of this common ocular disease. My name is Kim and I am a fourth year medical student at the University of [01:20] Alberta. I’d like to give a huge thanks to Dr. Chris Rudniski for his expert review of this content. Today’s objectives are to 1. Describe the eye anatomy relevant to glaucoma. 2. Understand the pathophysiology, symptoms, and management options for open-angle glaucoma. 3. [01:40] Understand the pathophysiology, symptoms, and management options for acute angle closure glaucoma and, four, list other causes of glaucoma. Definition. Glaucoma is a common eye disease. In glaucoma, patients get optic nerve damage. Glaucoma is associated with [02:00] high eye pressure inside the eye called intraocular pressure, or IOP. Not all cases of glaucoma have high IOP, but it is safe enough for this introductory discussion to think of glaucoma as optic nerve damage with elevated intraocular pressure. The [02:20] The cutoff measurement for high IOP is usually 21 millimeters of mercury. Anatomy. How can you even get high pressure inside the eye? To understand this, we need to discuss aqueous humor and the angle of the anterior chamber. Aqueous humor is the [02:40] that fills up the anterior chamber, which is the space between the cornea and the iris. Aqueous humor is constantly being produced and drained out of the eye, so IOP can rise if aqueous is not being drained effectively. The ciliary body, [03:00] behind the iris produces aqueous humor. You may know that the ciliary body’s second job is to anchor the zonules that suspend the lens. Let’s follow the path of aqueous humor in the eye. The ciliary body produces aqueous from here, aqueous flows in [03:20] front of the lens, forward through the pupil, and into the anterior chamber. From there, aqueous drains into the angle formed by the cornea and the iris into a drainage system called the trabecular meshwork. From the trabecular meshwork, aqueous makes its way into the venous [03:40] system of the body. As an aside, if you are loving this discussion of eye anatomy and physiology, check out our other Surgery 101 podcast episode on eye fundamentals. Open-angle glaucoma. In North America, by far the most common type of glaucoma is open [04:00] open angle glaucoma. This is the type that is screened for at optometry eye exams. You may have experienced the unpleasant puff of air onto your eye when you were looking at the hot air balloon picture. This is one way to measure eye pressure, or IOP. We screen for open angle glaucoma, OAG, [04:20] because most patients with OAG are asymptomatic and because OAG causes gradual vision loss if we don’t intervene with management. What do we mean by open angle? Remember that the angle that we’re talking about here is the angle in the anterior chamber between the core [04:40] Here, aqueous humor drains into the trabecular meshwork. In open-angle glaucoma, the angle is perfectly normal and not too narrow, so the reason for the high IOP isn’t that the drainage angle is closed. So if the angle is [05:00] fine in OAG, what’s causing the high intraocular pressure? The thought here is that with age, there is microscopic dysfunction or clogging of the trabecular meshwork. So in open-angle glaucoma, aqueous humor can’t drain effectively through the trabecular meshwork. [05:20] which raises IOP and damages the optic nerve. The three major findings of chronic open-angle glaucoma are 1. high IOP, 2. optic disc changes, and 3. visual field loss. Let’s break each of these down [05:40] before diving into treatment. As mentioned before, the cutoff for high intraocular pressure is an IOP greater than 21 millimeters of mercury. For optic disc changes, ophthalmologists train to notice subtle changes in the appearance of the optic disc that signify [06:00] damage from glaucoma. One of these is a cup to disc ratio greater than 0.5. The details of this cup to disc ratio are beyond this introductory episode. For visual fields, patients with OAG tend to lose their peripheral vision slowly over time. [06:20] This is why we check their visual fields. To do this, ask the patient to look at your nose and hold out your hands midway between the two of you, holding up either one, two, or five fingers, and ask the patient how many fingers they count. Make sure they’re always looking at your nose and not taking a peek. [06:40] off to the side where your hands are. You can assess how well they see in each quadrant of vision with each eye. Let’s look at management of open-ingle glaucoma. There are many medical treatment options in the form of eye drops that are first line. These include topical prostaglandin and [07:00] beta blockers, alpha agonists, and carbonic anhydrase inhibitors. Since this podcast is with Surgery 101, however, we will focus our discussion on understanding some surgical
Short Bowel Syndrome: Insights, Challenges, and Management Strategies
This podcast explores Short Bowel Syndrome (SBS), highlighting its causes, challenges, and management strategies. It covers medical and surgical options, nutrient absorption issues, complications, and treatment advancements to improve patient outcomes. Transcript [00:00] Hello and welcome back to Surgery 101. The podcast brought to you with the help of the Department of Surgery at the University of Alberta. By [00:20] My name is Jonathan White, coming to you from the Royal Alexandra Hospital here in Edmonton. In this week’s episode, we’ll be hearing from medical student Leanne Kim, who comes to us from McMaster University, and she’ll be considering the topic of short bile syndrome. Given the topic, we’re going to try to be brief. [00:40] you’ll be considering what the syndrome is, how we recognize it, how it works, what are the prognostic factors, and how we treat it. So let’s keep it short with Short Bile Syndrome here on Surgery 101. [01:00] Hello, my name is Leanne Kim and I’m a third year medical student at McMaster University. [01:20] Today we’ll be discussing short bowel syndrome. After listening to this podcast, listeners will be able to 1. define the term short bowel syndrome, SBS for short 2. recognize SBS in post-surgical patients 3. describe the pathophysiology of SBS [01:40] 4. List prognostic factors for SBS 5. Describe the basis and indications for medical and surgical therapy for SBS What is Short Ball Syndrome and why do you need to know about it? Short Ball Syndrome is defined as the impairment and absorption of macronutrients and micronutrients [02:00] from a small bowel due to an adequate length and absorptive surface. Although SBS can result from congenital defects and surgeries in pediatric patients, today we would like to focus on post-surgical SBS in adult patients. Normal length of the small bowel is 6 meters for adults. Adult patients with a small bowel length of less than [02:20] centimeter due to surgical resection or bypass are at high risk for SBS. Intestinal failure where the patient remains dependent on parenteral nutrition is more likely when the small bowel length is less than 60 centimeters. In general, up to 50% of patients are able to be weaned off parenteral nutrition within five years of diagnosis. [02:40] as to gastrointestinal mucosa undergoes compensatory remodeling. Usually the remaining length of the small bowel can be found in the OR nuts. Patients with SBS are found to have low quality of life index, chronic fatigue associated with frequent defecation, dehydration, as well as frequent care for parent [03:00] nutrition pump can interfere with their sleep. Moreover, SVS is associated with increased mobility and high healthcare costs as well. With that in mind, let’s dive in. Let’s look at a case. You’re on neurogeneral surgery rotation and in the follow-up clinic you meet Charles. Charles is a 55-year-old patient [03:20] who is dependent on home parenteral nutrition two years after the small bowel resection from acute mesenteric ischemia. Since the resection, he has not been able to tolerate internal nutrition due to abdominal cramping, bloating, and persistent watery diarrhea. He has lost about 15 pounds. You notice on his chart that he was hospitalized a few weeks [03:40] ago were catheter-associated sepsis. As this has been greatly impacting his life, he’s here to discuss possible medical or surgical options for his parenteral nutrition dependence. What are common causes of SBS? The causes of SBS depend on the underlying condition that requires surgical resection. [04:00] In adults, most common causes are acute mesenteric ischemia, malignancy, and Crohn’s disease. In patients with Crohn’s disease, SBS may develop over a series of resection. In pediatric patients, most common causes of SBS are intestinal atresia, valvulus, and necrotizing intercalation. [04:20] clinical presentation. Postoperative ileus, which refers to a decrease in bowel motility following a major abdominal surgery, usually results within 24 hours after small bowel surgery. Usually, passing a gas or stool indicate the resolution of postoperative ileus. [04:40] Enterol feeding is initiated once the isleist resolves, though recently there was a cochlear review that enterol nutrition within the first 24 hours after lower gastrointestinal surgery is associated with shorter length of hospital stay. Once the enterol nutrition is initiated, patients at risk for SBS may experience symptoms such as non-proliferation [05:00] blood watery diarrhea with increased transit time, anorexia, vomiting, bloating, and abdominal cramping. All of these elements should be characterized further systematically on history. On physical exam, the patient may be cacti, tachycardic, and appear dehydrated from ongoing intestinal loss of fluid, electrolytes, and [05:20] It is important to do thorodomol and volume setus exams. In post-surgical patients with watery diarrhea, a few differential diagnoses should be ruled out before making the final diagnosis of SBS. If the patient is fibril, it is important to roll out intraabdominal sepsis with further investigation. [05:40] Infectious colitis should also be ruled out with stool studies to ensure that the patient receives appropriate treatment. Let’s look at the case again. Charles had an extensive small bowel resection from acute mesenteric ischemia two years ago and since then has not been able to tolerate enteral nutrition, eutopdominal cramping, bloating, and persistent water [06:00] area. What is the pathophysiology of compensatory modeling in post-surgical patients? In the post-resection phase, decrease in absorptive surface for macronutrients and micronutrients contribute to persistent osmotic diarrhea and bloating. In the following months, compensatory structural and [06:20] physiological adaptations take place to increase uptake of nutrients and fluid. For instance, the crypt, death, and villus height are increased and optimized to maximize the surface area that is in contact with the luminal content. The crypt cells undergo proliferation and differentiation to replenish the enterocytes and tereundocrine cells called the cells and [06:40] cells. Such hyperplasia of the mucosa is accompanied by the angiogenesis to ensure effective nutrient delivery via the hepatic portal system. Gross changes such as bowel lengthening and dilation also take place. Of interest, glucagon-like peptide 2, GLP2 for short, is an anti-rheumatoid hormone that