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 is known to
[07:00] immediate intestinal hyperplasia. GLP2 will be discussed further later in the podcast. In addition to structural changes, physiological adaptations also play an important role. As an example, expression and maturation of the transporter, exchange of proteins, and brushboarder enzymes are augmented and accelerated. Moreover, the transit time increase
[07:20] increases and allows the luminal nutrients to be in contact with the ulcerative surface for a longer period of time. In summary, structural and physiological adaptations of the gastrointestinal mucosa can prevent or delay intestinal failure in post-surgical patients. Prognosis Although the length of the remaining small
[07:40] valve is useful in predicting the prognosis, there are other factors that need to be taken into account. First, the presence of intact aliozecal valve. The aliozecal valve is important for modulating the transit time. An intact aliozecal valve can extend the contact time for nutrient absorption. Second, the location of the resection. Resection
[08:00] the ilium is likely to result in less favorable outcome than the resection of the jejunum, as the iliums where the bowel, salt, and vitamin B12 are absorbed. The ilium also has been found to have greater capacity for intestinal adaptation than the jejunum. Third, the functional level of a small bowel and a colon. Having
[08:20] 50 cm of functional, residual small bowel would predict more favorable prognosis than mildly diseased residual bowel of the same thing. This explains why patients who had end-judgenostomy where the ilium and the ileosicle valve are resected are more likely to develop SBS and subsequently intestinal failure.
[08:40] Can patients be on permanent parenteral nutrition? What are the risks to being on permanent parenteral nutrition? Patients who are on permanent parenteral nutrition are an increased risk for catheter-associated sepsis, venous thrombosis, acalculus coasis status, and liver failure. Catheter-associated sepsis can occur in
[09:00] up to 10% of those receiving parenteral nutrition. Therefore, it is important to initiate parenteral nutrition early and wean the patient off parenteral nutrition if tolerated. Complications of SPS. Long standing loss of absorptive capacity in SPS can lead to multiple complications. First, calls to
[09:20] related disease. Absence of oral intake leads to gallbladder stasis. This, combined with impaired reabsorption of the bile acids from the ilium, can synergistically increase risk of gallstone formation. Second, osteoporosis. Low calcium absorption can promote bone reabsorption and eventually lead to osteoporosis.
[09:40] Third, kidney stones. Normally calcium binds to oxalate and the GI lumen. Lipids that have not been observed in the lumen can chelate calcium and lead to the free uptake of oxalate across the mucosa. The buildup of free oxalate can eventually lead to formation of oxalate stones in the kidney. These complications, compounded by complications
[10:00] secondary to administration of parenteral nutrition can lead to multiple comorbidities and increased mortality rate in these patients. Now that we have a better grasp pathophysiology of SPS as well as the pros and cons of parenteral nutrition, let us explore medical and surgical management options that we can suggest to Charles. Medical management
[10:20] As mentioned earlier, GLP2 is an antiramendocrine peptide hormone that mediates intestinal hyperplasia. It promotes crypt cell proliferation, blood flow, and nutrient absorption. Half life of endogenous GLP2 is limited by DPP4, which is an enzyme that degrades GLP2.
[10:40] Tetagglutide is a synthetic long-acting analog of GLP2 that is resistant to degradation by DPP4. In phase 3 clinical trials, Tetagglutide was shown to reduce the need for parenteral nutrition by 20%. In practice, Tetagglutide is considered in patients with dependence on parenteral nutrition for more than two years after the resection
[11:00] and or with previous complications secondary to parental nutrition. One contraindication to GLP2 therapy is actually GI malignancy. Therefore, colonoscopy is routinely performed to rule out GI malignancy before and after the tetrachlorotide therapy. Surgical management.
[11:20] If the patient has severe intestinal failure with associated liver disease, transplantation of the small bowel and the liver may be preferred over non-transplant surgical options. As with transplants, there is a risk of acute or chronic rejection. However, there is currently evolving literature that transplantation leads to high mortality and morbidity.
[11:40] Non-transplant options, which are also referred to as the autologous gastrointestinal reconstruction, can be considered in patients who meet the following criteria. One, dilated small intestine. Two, strong dependence on parenteral nutrition. Three, plateaued intestinal adaptation. Four, absence of GI motility disorder.
[12:00] disorder, five, absensive major surgical risks from previous vulnerabilities. In principle, these surgical approaches aim to lengthen the small bowel or increase transit time. One option is called the longitudinal intestinal lengthening and tailoring procedure, which is also known as a Lilt or Bianchi procedure.
[12:20] In this procedure, the small intestine is divided longitudinally and attached in isoparesptal fashion to create one passageway for the luminal content. This procedure is preferred in patients with uniform dilation of the small intestine to allow for uniform longitudinal division and subsequent anastomosis.
[12:40] from the little procedure include compromised intestinal blood flow, anesthemosis leak, and small bowel obstruction. Another option is called a serial transverse enteroplasty procedure, which is also known as the STEP for short. In STEP, staples are applied transversely in a serial fashion along the length of the small intestine.
[13:00] and create a zigzag shaped small intestine. This procedure prolongs transit time. Some complications of the step are small wall obstruction, stricture, and leakage from the stable line. If appropriate, step can be performed on patients in conjunction with the Bianchi procedure. Now back to Charles.
[13:20] After discussing with the multidisciplinary parental nutrition team, trials is recommended to do tetrachloro therapy and is scheduled for a colonoscopy to roll out GI malignancy in advance. Trials is happy to proceed with the suggested plan. The interdisciplinary team also considers that because trials has been on parental nutrition for more than two years, it will be
[13:40] challenging for trials to be completely independent with an enteroneutrition. They take time to discuss with trials the role of parenteral nutrition for patients with intestinal failure as well as risk and benefits of parenteral nutrition. Major takeaway points from today. One, Drouppard syndrome refers to decreased nutrient and
[14:00] absorption due to a significant resection of the small intestine. 2. The residual length, presence of the isilosacryl valve, anatomical location of the resection, as well as the functional level of the residual small intestine determine the likelihood of SBS in post-surgical patients. 3. Prolonged parental penetration is not
[14:20] without complications. And if the patient becomes dependent on parental nutrition, medical options such as tetraglutide or surgical options such as lilt or step can be considered to decrease mortality and enhance the patient’s quality of life. Thank you for listening to this week’s Surgery 101 podcast. I want to thank Dr. White and Ms.
[14:40] Michelle Lindbergh as well as Dr. Leah Gramlich for their support for the development of this podcast. Hope you found this podcast helpful and informative.
[15:00] Thanks for that excellent overview. That’s all we have for this week. So thanks for listening and we’ll see you back here next week on Surgery 101.
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