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