Dispatches from the GUILD Conference, Series #68

Eosinophilic Esophagitis: Tips for the Primary Care Provider

May 2025 • Volume XLIX, Issue 5
Evan S. Dellon

Read Article

Eosinophilic esophagitis (EoE) is a chronic allergic clinicopathologic condition with a rapidly increasing incidence and prevalence and is being increasingly seen in both specialty and primary care settings. Left untreated, EoE progresses from an inflammation-predominant to fibrostenotic condition in most patients. Diagnosis requires a combination of clinical symptoms, esophageal eosinophilia on biopsies obtained during upper endoscopy, and exclusion of other potential causes of eosinophilia. Treatments include dietary elimination, medications (proton pump inhibitors, swallowed/topical steroids, or biologics), and esophageal dilation (when strictures are present). Long-term therapy and monitoring are also required. This review discusses how commonly EoE is seen in the primary care setting, when to suspect a diagnosis of EoE, how EoE is treated, and how primary and specialty care can intersect management of this chronic disease; practical tips for the primary care provider are also presented.

Introduction

Eosinophilic esophagitis (EoE), a chronic allergic condition first described about three decades ago, has transitioned from a rare and case-reportable disease to one that is being increasingly seen, not just in gastroenterology and allergy specialty settings, but in the primary care setting as well. EoE is defined as a clinicopathologic disease, meaning that diagnosis requires both clinical symptoms and the presence of esophageal eosinophilia.1 Similar to asthma and atopic dermatitis, EoE is a type 2 inflammatory condition, and the current pathogenic model holds that food or environmental allergens interact with an impaired esophageal epithelial barrier, which then triggers a T-cell mediated cascade of typical allergic cytokines and mediators resulting in accumulation of eosinophils and mast cells in the esophagus, activation of fibroblasts, and esophageal remodeling.2 Left untreated, EoE will progress from an inflammation-predominant to fibrostenotic condition in most patients, with complications including food impaction, esophageal stricture, and, in children, poor growth and nutrition.3 There are multiple treatment options for EoE, with more in the drug development pipeline, and patients require long-term therapy and monitoring. This review will discuss how commonly EoE is seen in the primary care setting, when to suspect a diagnosis of EoE, how EoE is treated and how primary and specialty care can intersect management of this chronic disease. It also presents practical tips for the primary care provider. (Table 1)

How Commonly is EoE Seen in Primary Practice Settings?

The incidence of EoE has been rising at a rate that outpaces increases in awareness and frequency of performing endoscopy and biopsy, suggesting ongoing environmental changes are driving this disease.3 Because the condition is chronic and does not increase mortality, prevalence has been rapidly rising as well. Fifteen years ago, the prevalence was ~1/2000, but the most recent estimates are 1/700 with almost a half million diagnosed cases in the U.S.4 However, this might only be the tip of the iceberg, as recent studies suggest there is likely a large undiagnosed EoE patient population that could double to triple the current prevalence,5 as well as a long delay between symptom onset and diagnosis.6

The implication of this rising prevalence is that primary care providers will see known EoE patients in clinic as well as symptomatic patients who may yet to be diagnosed. In addition, the prevalence of EoE is quite a bit higher in certain populations.3 For patients undergoing upper endoscopy (EGD) for any reason (including open access referrals), the prevalence may be ~5%; for those undergoing EGD for dysphagia, the prevalence could be as high as 20-25%; for those who have a food impaction and require an emergency department visit, the prevalence is >50%. Additionally, patients with other atopic conditions have an increased prevalence of EoE as well,7 and this can be an important clue when considering EoE diagnosis, as below.

When Should Primary Providers Suspect EoE as a Diagnosis?

The symptoms of EoE are not pathognomonic, which can make diagnosis challenging. In adolescents and adults, dysphagia is the hallmark symptom. However, many patients may not realize or report they are having trouble swallowing (outside of an overt food impaction) because symptom onset can be slow in EoE, and patients can subconsciously adapt their eating behaviors to minimize symptoms. This is highlighted by the “IMPACT” acronym,8 where they “Imbibe” a lot of fluids while eating to help food go down; “Modify” foods by cutting into small pieces, lubricating foods, or pureeing; “Prolong” meal times by eating slowly or are the last one at the table; “Avoid” foods that might get stuck; “Chew” excessively to make food mushy and easy to swallow; or “Turn away” tablets or pills, as not being able to swallow pills or having pills stick is a subtle but common symptom. Therefore, for patients with reported or suspected dysphagia, asking specifically about the IMPACT symptoms can increase the suspicion for EoE, highlight a substantial burden of symptoms, and facilitate diagnosis. Other symptoms in adolescents and adults can include atypical chest pain and heartburn which is often unresponsive to antiacid therapy. Prior to referring a patient with refractory gastroesophageal reflux disease (GERD) for anti-reflux surgery, EoE should be excluded as it is a cause of refractory reflux symptoms in a few percent of patients.3 For children, symptoms are also non-specific. Infants and toddlers can have failure-to-thrive and poor growth or feeding difficulties such as failure to progress with consistencies. In school age children, abdominal pain and vomiting are common, and it is important to distinguish if vomiting is “true” vomiting or a manifestation of regurgitation of food stuck in the esophagus.  Symptoms of chest pain, reflux, and heartburn can also be seen in this age group.

While EoE is on the differential diagnosis for all of these symptoms, what can increase the suspicion of EoE on a practical basis? First, if a patient has concomitant atopic conditions, such as asthma, eczema, immediate type (IgE-mediated) food allergies, or allergic rhinitis, in the presence of upper GI symptoms (or feeding issues for younger children), EoE should rise on the differential diagnosis. This is because there is a marked increase of EoE in patients with atopic disease.7 For example, 5% of children with food allergies can have EoE,9 and the more atopic conditions in one patient, the higher the chance of EoE (>10% with 3 or more allergic diseases).10 Similarly, if a patient has reported food impaction, then EoE should be suspected. While the general perception is that EoE is more common in younger patients, and in white males, it can affect patients of any age, sex, race, or ethnicity.3 Predictive models have been developed for both adults and children,11,12 and an online calculator is available for adults to help understand the potential for EoE in a given patient (https://gicenter.med.unc.edu/cedas/index.php?page=CtrlNewEOE&action=showNewEOE).

How is EoE Diagnosed?

In order to diagnose EoE, a patient needs to have appropriate symptoms (as discussed above), at least 15 eosinophils per high-power field (eos/hpf) on esophageal biopsy obtained during upper endoscopy, and no other conditions that could cause esophageal eosinophilia.1 Therefore, EGD with biopsy is currently required for EoE diagnosis; there are no non-invasive methods currently available.  In the primary care setting, when EoE is suspected, referral to a gastroenterologist or for open access endoscopy should be made. In addition, the suspicion of EoE should be specifically mentioned. For open access endoscopy, while it is guideline-recommended to obtain esophageal biopsies for procedures done for an indication of dysphagia,13 if there are less typical symptoms, biopsies may not always be taken and a diagnosis could be missed. When a gastroenterologist performs an upper endoscopy and EoE is suspected, the key endoscopic findings of EoE, though not part of the diagnostic criteria, will increase the possibility of the diagnosis.14 These include esophageal edema (decreased vascularity), fixed rings, exudates (white plaques), furrows (longitudinal lines), stricture, narrowing, or crepe-paper mucosa (a sign of mucosal fragility). (Figure 1) It is recommended that the most common findings (edema, rings, exudates, furrows, and stricture) are reported using the EoE Endoscopic Reference Score (EREFS),15 which typically ranges 0-9 with higher scores indicating more severe findings, and which can be followed in addition to biopsy results to track treatment response. Once EoE is diagnosed, initial management is usually done by the gastroenterologist or an allergist. The diagnosis may also be suspected by an allergist, and an allergist is important to help manage the concomitant allergic conditions associated with EoE.

Table 1. Tips For Primary Care Providers Related to Eosinophilic Esophagitis

TipRationale
Expect to see patients with EoE as it is no longer a rare diseaseThe incidence and prevalence of EoE continue to rapidly rise
Ask about more than trouble swallowingPatients will often modify their eating with adaptive strategies, which can be highlighted on history by asking about the “IMPACT” behaviors
Think about EoE in patients with allergic conditions
and upper GI symptoms		EoE is more common in patients with allergic conditions than in the general population, and the more allergic conditions that are present, the more likely a diagnosis of EoE will be
Consider whether a report of an “allergic reaction” to
a food might be due to a transient food impaction		Patients may interpret food getting stuck (with associated discomfort, hypersalivation, and perceived trouble breathing or anxiety) as an allergic reaction, when in fact it is a sign of EoE
Refer to a gastroenterologist for upper endoscopy
and biopsy to diagnose EoE		While diagnosis requires the correct clinical symptoms, it also requires demonstration of esophageal eosinophilia (at least 15 eos/hpf), which requires upper endoscopy and biopsy for assessment
Refer to an allergist for management of multiple concomitant atopic conditionsConcomitant atopic conditions are seen in 60-80% of patients with EoE, and allergists are key members of the multidisciplinary team required for optimal EoE management
Assess disease activity by considering multiple domains including symptoms, endoscopic features, and histologic findingsIt is not sufficient to monitor symptoms alone in EoE, as symptoms are often discordant with biologic disease activity noted on endoscopy and histology, so all three domains should be assessed
Some topical steroid treatments for EoE adapt asthma preparation and might appear to duplicate other medications
on patients’ medication lists		Budesonide and fluticasone have traditionally been swallowed (rather than inhaled from asthma devices), and at different doses than used for asthma; while there is an FDA-approved budesonide now available for EoE, it is important to assess EoE medications (which also include PPIs and dupilumab) to make sure the dosing and use is correct for a given indication

How is EoE Treated?

Goals of EoE treatment are to decrease symptoms, improve endoscopic and histologic findings, normalize growth and nutrition, and prevent complications such as esophageal stricture, food impaction, and esophageal perforation. Guidelines recommend a treatment approach where an anti-inflammatory option is paired with esophageal dilation of strictures, when they are present and cause dysphagia.16 Initial anti-inflammatory options include pharmacologic and dietary therapies, and a shared decision-making framework is recommended for a patient to select a treatment. Dietary elimination is based on food allergens causing EoE in the majority of patients.17 However, because current allergy tests (e.g. skin prick, blood IgE or IgG testing) do not correlate with food triggers in EoE, performing these is not recommended.16 Instead, an empiric elimination diet that removes the most common food triggers of EoE is the first step. These can be less restrictive (removing dairy only, or dairy and wheat), or more restrictive depending on patient preference.17 Initial medication options include proton pump inhibitors (PPIs) and topical or swallowed corticosteroids (tCS). Though off-label, PPIs are effective in ~30-40% of patients and work via non-acid-dependent mechanisms, so it is important to explain to patients that they are not using them for the typical GERD indication.18 tCS coat the esophagus to provide a local effect, and are effective in 50-70% of patients.19 Traditionally, budesonide or fluticasone asthma preparations were modified to be swallowed off-label, but recently a budesonide oral suspension has been FDA-approved for treatment of EoE.20 For patients who do not respond to these medications, the FDA-approved biologic dupilumab21 can be considered as step-up therapy in most cases; in some patients with severe atopic conditions that would warrant dupilumab use, the medication can be considered earlier in the treatment algorithm.16

How is EoE Managed Long-Term and How Does this Intersect with Primary Care?

After an initial treatment is selected, repeat upper endoscopy and biopsy should be performed to assess response.16 If there is no response to first-line therapy, treatment can be switched or escalated and then endoscopy is repeated. When a response is achieved, and the goal is improvement across symptom, endoscopic, and histologic domains, the treatment should be maintained long term.22  Data from multiple sources demonstrate that when treatment is stopped in EoE the disease activity universally recurs, with many patients flaring as soon as three months. In addition, in contrast to some other atopic diseases, patients do not “grow out of EoE”.22

Long-term EoE care, while often requiring GI or allergist input and monitoring, may overlap with the primary care setting. When patients with EoE come to clinic, it is important to know what medications or diet elimination they are on and what the rationale is for each treatment so adherence can be assessed and refills provided if necessary. For diet, the distinction between food elimination for EoE and food elimination for an immediate-type food allergy is important. In the latter case, foods cannot be added and any amount can trigger a severe reaction; in EoE, strict elimination is needed for disease control, but inadvertent exposure to a food trigger will not cause immediate harm. Further, because some medications like PPIs, budesonide, and dupilumab have multiple uses and doses differ across diseases, it is important to understand which is being used for EoE, whether it is at the appropriate dose, and whether it is doing “double duty” for a different condition. Finally, EoE is often managed in a multidisciplinary way, with allergists, gastroenterologists, pathologists, dieticians, feeding therapists, psychologists, and others contributing to care, and this group, which is typically not in the same clinic, can be coordinated by the primary provider.

Conclusions

EoE is a chronic allergy/inflammatory condition of the esophagus that is rapidly rising in incidence and prevalence and is still likely underdiagnosed. A primary care provider will therefore encounter an increasing number of patients with established EoE as well as patients with symptoms suggestive of EoE, and can play a major role in facilitating diagnosis. Situations that can increase the suspicion of EoE in clinic go beyond typical adolescent/adult symptoms of dysphagia and food impactions, to the “IMPACT” adaptive eating behaviors, and to patients with atopic conditions who also have upper GI symptoms. Prompt referral to GI for endoscopy and biopsy, with specific mention of the concern for EoE, is needed for timely diagnosis. While the initial treatment and monitoring of EoE are often performed by GI and allergy, long-term monitoring and reinforcement of appropriate treatment strategies can also be achieved in the primary care setting. 

References

1. Dellon ES, Liacouras CA, Molina-Infante J, et al. Updated international consensus diagnostic criteria for eosinophilic esophagitis: Proceedings of the AGREE conference. Gastroenterology. 2018;155:1022-33.e10. Epub 2018/07/17.

2. Kennedy KV, Muir AB, Ruffner MA. Pathophysiology of Eosinophilic Esophagitis. Immunol Allergy Clin North Am. 2024;44(2):119-28. Epub 2024/04/05.

3. Dellon ES, Hirano I. Epidemiology and Natural History of Eosinophilic Esophagitis. Gastroenterology. 2018;154:319-22.e3. Epub 2017/08/05.

4. Thel HL, Anderson C, Xue AZ, et al. Prevalence and Costs of Eosinophilic Esophagitis in the United States. Clin Gastroenterol Hepatol. 2024. Epub 2024/11/02 23:12.

5. Lam AY, Lee JK, Coward S, et al. Epidemiologic Burden and Projections for Eosinophilic Esophagitis-Associated Emergency Department Visits in the United States: 2009-2030. Clin Gastroenterol Hepatol. 2023. Epub 2023/05/11.

6. Reed CC, Koutlas NT, Robey BS, et al. Prolonged Time to Diagnosis of Eosinophilic Esophagitis Despite Increasing Knowledge of the Disease. Clin Gastroenterol Hepatol. 2018;16(10):1667-9. Epub 2018/01/29.

7. Weir AA, Iweala OI, Dellon ES. High prevalence of eosinophilic gastrointestinal disorders in patients with atopic disease. Ann Allergy Asthma Immunol. 2024. Epub 2024/12/10.

8. Hirano I, Furuta GT. Approaches and Challenges to Management of Pediatric and Adult Patients With Eosinophilic Esophagitis. Gastroenterology. 2020;158(4):840-51. Epub 2019/12/15.

9. Hill DA, Dudley JW, Spergel JM. The Prevalence of Eosinophilic Esophagitis in Pediatric Patients with IgE-Mediated Food Allergy. J Allergy Clin Immunol Pract. 2017;5(369-375). Epub 2017/01/04.

10. Hill DA, Grundmeier RW, Ramos M, et al. Eosinophilic Esophagitis Is a Late Manifestation of the Allergic March. J Allergy Clin Immunol Pract. 2018;6(5):1528-33. Epub 2018/06/30.

11. Cotton CC, Betancourt R, Randall C, et al. A Model Using Clinical and Endoscopic Characteristics Identifies Patients at Risk for Eosinophilic Esophagitis According to Updated Diagnostic Guidelines. Clin Gastroenterol Hepatol. 2021;19:1824-34.e2. Epub 2020/07/08.

12. Borinsky SA, Miller TL, Dellon ES. A clinical predictive model identifies pediatric patients at risk for eosinophilic esophagitis. Dig Liver Dis. 2024;56(12):2045-51. Epub 2024/07/08.

13. Aceves SS, Alexander JA, Baron TH, et al. Endoscopic approach to eosinophilic esophagitis: American Society for Gastrointestinal Endoscopy Consensus Conference. Gastrointest Endosc. 2022;96(4):576-92.e1. Epub 2022/08/15.

14. Kim HP, Vance RB, Shaheen NJ, et al. The Prevalence and Diagnostic Utility of Endoscopic Features of Eosinophilic Esophagitis: A Meta-Analysis. Clin Gastroenterol Hepatol. 2012;10:988-96.e5.

15. Hirano I, Moy N, Heckman MG, et al. Endoscopic assessment of the oesophageal features of eosinophilic oesophagitis: validation of a novel classification and grading system. Gut. 2013;62:489-95. Epub 2012/05/24.

16. Dellon ES, Muir AB, Katzka DA, et al. ACG Clinical Guideline: Diagnosis and Management of Eosinophilic Esophagitis. Am J Gastroenterol. In press, 2025.

17. Chang JW, Kliewer K, Haller E, et al. Development of a Practical Guide to Implement and Monitor Diet Therapy for Eosinophilic Esophagitis. Clin Gastroenterol Hepatol. 2023;21:1690-8. Epub 2023/03/19.

18. Franciosi JP, Mougey EB, Dellon ES, et al. Proton Pump Inhibitor Therapy for Eosinophilic Esophagitis: History, Mechanisms, Efficacy, and Future Directions. J Asthma Allergy. 2022;15:281-302. Epub 2022/03/08.

19. Franciosi JP, Gordon M, Sinopoulou V, et al. Medical treatment of eosinophilic esophagitis. Cochrane Database Syst Rev. 2023;7(7):Cd004065. Epub 2023/07/20.

20. Hirano I, Collins MH, Katzka DA, et al. Budesonide Oral Suspension Improves Outcomes in Patients With Eosinophilic Esophagitis: Results from a Phase 3 Trial. Clin Gastroenterol Hepatol. 2022;20:525-34.e10. Epub 2021/04/23.

21. Dellon ES, Rothenberg ME, Collins MH, et al. Dupilumab in Adults and Adolescents with Eosinophilic Esophagitis. N Engl J Med. 2022;387(25):2317-30. Epub 2022/12/23.

22. von Arnim U, Biedermann L, Aceves SS, et al. Monitoring Patients With Eosinophilic Esophagitis in Routine Clinical Practice – International Expert Recommendations. Clin Gastroenterol Hepatol. 2023;21:2526-33. Epub 2022/12/27.

Download Tables, Images & References

Nutrition Reviews in Gastroenterology, SERIES #23

Kidney Stones in Short Bowel Syndrome: Causes and Preventive Measures 

May 2025 • Volume XLIX, Issue 5
Melanie Betz

Read Article

Short bowel syndrome (SBS) occurs from either surgical resection or malfunction of a significant amount of small bowel. An estimated 42-50% of patients with SBS will develop kidney stones in their lifetime.1,2 Both uric acid and calcium oxalate stones are common. Increased kidney stone risk stems from a combination of possible factors including inability to maintain adequate hydration, reduced alkali absorption, enteric hyperoxaluria, hypomagnesemia, altered gut microbiome, and poor food and beverage intake. Treatment must be individualized to each patient’s 24-hour urine collection results as the cause of kidney stones will differ based on etiology of SBS and natural variations. Evidence based treatments for stone prevention in SBS include improving hydration status, oral calcium to reduce oxalate absorption, reducing dietary fat and/or oxalate, alkali supplementation, and the correction of hypomagnesemia. Dietary recommendations should be made by a registered dietitian after a complete nutrition assessment to ensure the recommendations are appropriate.

Introduction

Short bowel syndrome (SBS) is defined as “a clinical condition associated to having less than 200 centimeters of residual small bowel (SB) in continuity, measured from the duodenojejunal flexure (ligament of Treitz), with or without colon, in an adult and for children (<18 years), less than 25% of the normal length SB for their respective age.” 3 SBS can result when  surgical resection of the bowel  leaves the remaining bowel with an insufficient length to support adequate digestion and absorption of oral nutrients. Additionally, SBS can occur as a consequence from dysfunction from the remaining bowel, even if the length is sufficient.  Most often,  SBS arises due to bowel resection resulting from trauma, inflammation, or ischemia; congenital disorders; or resulting from bariatric surgery.4

The most significant concern with SBS is malabsorption, making it challenging to maintain adequate nutrition and hydration. The extent of malabsorption largely depends on the length and location of the remaining bowel. If less than 50% of the SB is removed, the remaining bowel can adapt, minimizing risk of long-term complications.4 Complications of SBS include high volume stool or ostomy output, fluid and electrolyte imbalances, vitamin and mineral deficiencies, bone disease, hepatobiliary diseases, kidney stones, small intestinal bacterial overgrowth, and possibly the need for parenteral support.4,5 This review will focus on mechanisms of how SBS increases the risk of kidney stones and the nutrition therapies for its prevention.

Prevalence of Kidney Stones 

Kidney stones occur in 43-50% of patients with SBS.1,2 This is remarkably higher than the estimated 10% of the general population with kidney stones.6 Reduced kidney function is also common; one study found 28% of patients with SBS developed some level of renal impairment.7 Kidney stones, along with infections and dehydration are likely responsible for kidney damage.

Both uric acid and calcium oxalate kidney stones are common in SBS, highlighting the need for metabolic urine testing to direct prevention.8,9 Patients with a SB ostomy may be at greatest risk of uric acid stones due to massive bicarbonate loss, leading to acidic urine and those with some colon-in-continuity are at higher risk of developing calcium oxalate stones.1,10

Mechanism of Stone Formation 

Kidney stones are prevalent in SBS due to a combination of factors stemming from malabsorption and dehydration. The exact cause of stone formation is different for each patient depending on the amount and location of bowel that is remaining and natural variations across people. 

Reduced Fluid Absorption 

The hallmark of SBS is high volume stool or ostomy output and difficulty maintaining hydration due to endogenous losses of both fluid and electrolytes. Additionally, poor appetite and GI symptoms related to eating and drinking can contribute to reduced fluid intake. Limited absorption/resorption of oral fluids and endogenous secretions are problematic in many with SBS and often leads to reduced urine volume and increased saturation of lithogenic compounds. Reducing urine saturation is key to prevent all types of kidney stones.

Patients with a proximal SB ostomy have the most difficulty with enteric fluid absorption and often struggle with chronic dehydration leading to kidney injury and kidney stones.10 Patients with SBS that have their distal ileum and/or some colon-in-continuity tend to have more efficient fluid absorption and higher urine output, though risk for dehydration persists as rapid transit of fluid through the remnant SB may exceed the absorptive capacity of the remnant SB and colon.

Inhibited Intestinal Alkali Absorption

A key tenet of calcium kidney stone prevention is maintenance of adequate urine citrate. Citrate complexes with calcium to form a soluble compound in the urine, reducing calcium available to complex with other compounds to form kidney stones.11 Kidney stone prevention may include alkalizing urine pH via medications such as potassium citrate or sodium bicarbonate and reducing the dietary acid load.11,12 Urine alkalization helps prevent uric acid stones as low urine pH is the biggest driver of uric acid kidney stone formation. For calcium-based stones, dietary or medicinal alkali helps increase urine citrate as well as alkalize urine, which may help prevent calcium oxalate kidney stone formation.

Patients with SBS tend to have low urine pH and low urine citrate, increasing risk of both uric acid and oxalate kidney stones.10 In SBS, alkali precursors such as potassium, magnesium and calcium are poorly absorbed by the residual SB, which may result in highly acidic urine predisposing patients to uric acid kidney stones.10 In addition, when alkali is not absorbed by the GI tract – from either alkali malabsorption or a high dietary acid load – the kidney will reabsorb more citrate to buffer the higher acid load, resulting in lower urine citrate.10 Examples of dietary sources of alkali and acid precursors and exact potential renal acid load (PRAL) values are provided in Table 1. 

Enteric Hyperoxaluria

In non-stone formers, only 5-10% of dietary oxalate is absorbed. This varies widely based on dietary intake of calcium, fiber and other nutritional factors.13 The more calcium consumed, the more calcium binds with dietary oxalate in the gut causing reduced oxalate absorption and ultimately lower urine oxalate. By this mechanism, adequate dietary calcium is widely known to reduce the risk of forming oxalate kidney stones.14

Enteric hyperoxaluria is the over absorption of oxalate from the colon and can develop whenever fat malabsorption is present.15 Malabsorbed fat sequesters calcium in the SB, leaving oxalate to be absorbed in the colon and excreted in urine.15 Given the high frequency of fat malabsorption in SBS, enteric hyperoxaluria is common. The extent of bowel resection or dysfunction is correlated with the extent of hyperoxaluria.10 Enteric hyperoxaluria is of particular concern for patients with SBS that have partial or complete colon-in-continuity as oxalate is exclusively absorbed in the colon.10 There is very little risk of enteric hyperoxaluria in those with a SB ostomy (without colon-in-continuity). 

Hypomagnesemia 

Magnesium is a novel target for oxalate kidney stone prevention due to its ability to bind oxalate both in the intestine and urine to create a soluble complex. Both blood and urine magnesium levels tend to be lower in stone formers.16,17 Hypomagnesemia is common in patients with
SBS, especially in those without the distal ileum, where a majority of magnesium absorption occurs and likely contributes to risk of oxalate kidney stone formation.5 

A 2024 study found that magnesium supplementation reduced urine oxalate in individuals  with elevated baseline urine oxalate levels.18  However, in SBS, oral magnesium supplementation can worsen GI fluid losses, increasing stool/ostomy output, and thus worsening dehydration with increased risk of stone formation. Therefore, oral magnesium supplementation should be monitored closely, dose adjusted, and if necessary transitioned to parenteral supplementation to optimize fluid balance and serum magnesium levels.

Altered Gut Microbiome

There is a clear role of the gut microbiome in kidney stone formation.19,20 Most of the research has focused on the role that oxalate degrading bacteria play on reducing urine oxalate and therefore reduce oxalate kidney stone risk. The gut microbiome is altered in SBS, likely as a result of both dietary and physiological changes; it is likely that the alteration of the gut microbiome contributes to the increased prevalence of kidney stone formation. More research is needed to determine how and if the gut microbiome can be modulated to reduce kidney stone formation in patients with SBS.

Table 1. Dietary Sources of Alkali and Acid Precursors

Dietary PrecursorsPotential Renal Acid Load (mEq)
Alkali Producing Foods
All Fruits Examples:
Banana (1 medium)8.2
Blueberries (1 cup)1.5
Peach (1 each)4.7
All Vegetables  Examples:
Broccoli (1 cup, cooked)5.5
Green Beans (1 cup, cooked)3.5
Tomato (1/2 cup, raw)3.7
Acid Producing Foods
All Meat & Seafood Examples
Beef (4oz, cooked)12.9
Chicken (4oz, cooked)16.3
Cod (4oz, cooked)13.5
Most Cheeses
Example:
Cheddar Cheese3.5
Minimal Acid or Alkali Production Potential
Most Beans, Nuts, Seeds,  Legumes & Plant Protein Foods Examples:
Black Beans (1/2 cup, cooked)2.6
Lentils (1/2 cup, cooked)1.5
Walnuts (1/2 cup)1.7
Grains Examples:
Whole Grain Bread (1 slice)1.8
White Bread (1 slice)0.8
Brown Rice (1/2 cup cooked)2.2
Fats & Oils Examples:
Olive oil (1 tablespoon)0.0
Butter (1 tablespoon)0.1
Milk & Yogurt Examples:
2% milk (1 cup)1.5
Low Fat Yogurt (1 cup)0.4

Poor Oral Intake

Patients with SBS may control their stool output by limiting oral intake. As stated above, low volume of oral fluid intake contributes to dehydration, low urine volume, and kidney stone risk. Additionally, an unbalanced diet that is low in alkali precursors (fruits and vegetables) along with nutrient malabsorption can exacerbate low urine citrate and pH, all contributing to the risk of kidney stone formation.

Prevention and Treatment of Kidney Stones 

Given the complexity and variation of kidney stones in patients with SBS, it is crucial to individualize interventions to prevent stone formation based on 24-hour urine collections. Table 2 provides suggested interventions based on common urine risk factors for kidney stone formation.

Improve Hydration

The American Urological Association recommends consuming  adequate fluid to produce at least 2 ½ liters of urine output/day for kidney stone prevention.11 This volume of urine may be difficult to achieve for patients with SBS as increase in oral fluid intake often results in higher ostomy/stool output with reduced urine volume. Patients with SBS and low urine output (e.g., <1200 mL/24-hours) should be encouraged to sip fluids slowly throughout the day and to periodically measure 24- hour urine volume in response to oral fluid intake; small increases in urine volume can incrementally reduce kidney stone risk despite not producing the recommended amount of urine.

Table 2.
Kidney Stone Prevention Interventions Based on 24-hr Urine Collection Parameters

Urine Collection ResultDiet and Hydration Strategies
Low urine volume (<2.5 liters)• Increased oral fluids, ideally from water or unsweetened beverages
• Oral rehydration solution as appropriate
• IV fluids as appropriate 
• Avoid dietary sodium restriction 
• Avoid excess simple carbohydrate
Hyperoxaluria• Supplemental calcium of 200-300mg/meal to be taken with meals (if no hypercalciuria)
• Increase intake of calcium-rich foods with meals for a total of 1,000-1,200mg calcium/day
• Limit intake of very high oxalate foods
• Consider low fat diet (20-30% calories from fat) • Trial bile acid sequestrant
Low urine pH
or citrate		• Potassium citrate, sodium bicarbonate or other citrate supplements dosed based on 24-hour urine collection pH and citrate
• Consider increased dietary alkali
Hypomagnesemia• Supplementation of 300-400mg/day as necessary
• Monitor for increased GI losses

Some patients with SBS, especially those with SB ostomy, can benefit from drinking oral rehydration solutions (ORS). ORS are iso-osmolar glucose-electrolyte solutions that utilize the sodium-glucose transport mechanism to pull water across the SB mucosa and help to correct fluid and electrolyte losses. Patients can purchase ORS products or make ORS at home (Table 3). In some cases, parenteral fluids are necessary to maintain adequate hydration and increase urine volume.

For those with SBS, avoidance of excess simple sugar is recommended to prevent rapid emptying of hypertonic fluid into the proximal SB; this results in jejunal water secretion to dilute the chyme to isotonicity, and often causes osmotic diarrhea with a net fluid loss (a.k.a. dumping syndrome). This is particularly important for individuals without the terminal ileum and/or cecum as these are the normal sites of significant fluid reabsorption. It is also advisable to avoid sugar-laden beverages (e.g., fruit juices, sodas), oral nutrition supplements, and concentrated sweets (e.g., cookies, cake, ice cream) to reduce the osmotic effect on the SB.

Dietary Sodium

Typically, a limit of 2,300 mg of sodium per day is recommended for calcium stone prevention for those with high urine calcium as higher dietary sodium increases renal excretion of calcium.11 However, in SBS, especially for patients with a sodium wasting SB ostomy, dietary sodium should be unrestricted to promote water absorption, urinary fluid output, and to prevent hyponatremia related to sodium loss in ostomy effluent.

Low Fat Diet

If a patient with SBS has enteric hyperoxaluria, avoiding excess dietary fat can help reduce sequestration of calcium and thereby reduce the absorption of oxalate and urine oxalate. The American Society of Parenteral and Enteral Nutrition (ASPEN) recommends 20-30% of calories from fat for patients with SBS and colon-in-continuity.4 This does not eliminate fat from the diet and allows for 44-67 grams fat/day on a 2,000 calorie diet. It is important to have a registered dietitian assess a patient’s habitual diet to determine the need for dietary changes.

Alkali Supplementation

As stated above, a major cause of kidney stones in SBS is limited absorption of alkali leading to acidic urine and low urine pH. Given the reduced absorptive capacity of alkali for patients with SBS, it is unlikely that reducing the dietary acid load will significantly impact urine citrate or pH levels. In fact, Bianco et al. found that clinical advice to increase dietary alkali to patients with SBS did not raise urine pH, but prescriptive, oral supplementation of alkali and citrate did increase urine pH (0.34 ± 0.53 vs. 0.22 ± 0.55, p=0.26 and 83 ± 256mg/day vs. 98± 166mg/day, p= 0.74, respectively).21

Table 3.
Commercial and Homemade Oral Rehydration Solutions 

Commercially Available Powders and LiquidsHomemade Beverage Recipes
Ceralyte 70®Ingredients:
• 1 liter water
• 6 teaspoons sugar
• ½ teaspoon salt Instructions: Combine all ingredients and mix until completely dissolved Add sugar-free flavoring as needed Refrigerate Sip throughout the day
Drip Drop® Fast HydrationIngredients:
• ¾ cup fruit juice
• 3 ¼ cups water
• ¾ teaspoon table salt
Instructions: Combine all ingredients and mix until completely dissolved  Refrigerate Sip throughout the day
Liquid IV® Hydration MultiplierIngredients:
• 2 ½ cups tomato juice
• 1 ½ cups water
Instructions: Combine ingredients  Refrigerate  Sip throughout the day
Trioral® Rehydration Electrolyte PowderIngredients:
• 2 packets of Gatorlyte® powder
• 4 cups of water
• ¼ teaspoon of table salt
Instructions: Combine all ingredients and mix until completely dissolved  Refrigerate Sip throughout the day
Note: Patients with SBS should drink the sugar-containing oral rehydration solutions (ORS) to most efficiently promote water absorption. Do not add ice to chill ORS as it will dilute the solution changing the sodium and sugar concentration to less favorable levels.

Oral supplementation of citrate is the most common strategy to increase urine pH and citrate levels for patients with SBS. Potassium citrate and sodium bicarbonate are most commonly prescribed. If not tolerated, over the counter citrate supplements such as Moonstone® or Litholyte® can be used in place of prescription alkali, at the discretion of the physician, to ensure adequate alkali absorption, based on 24-hour urine collection results. It is important to periodically monitor 24-hour urine collection results to determine adequacy of dosing. 

Dietary Calcium

In the general kidney stone population, avoidance of calcium supplements is typically recommended due to concern about exacerbating hypercalciuria, especially when calcium supplements are taken away from meals.11,22 However, in patients with SBS, urine calcium is typically not elevated and calcium supplements with meals may help reduce oxalate absorption. All forms of calcium supplements can reduce oxalate absorption.

For those with SBS, including foods high in calcium, or taking calcium supplements, with each meal can help to reduce intestinal oxalate absorption, reduce urine calcium levels, and ultimately reduce oxalate kidney stone formation.13 For those with SBS and risk of kidney stones it is recommend they take 600-2000 mg per day, in split doses, with meals, e.g. 400-500 mg calcium per meal.20

Dietary Oxalate

Limiting dietary oxalate is frequently recommended for patients with SBS to reduce their urine oxalate levels. However, there is debate as to whether a low oxalate diet is beneficial for oxalate stone prevention due to the inevitable restriction of beneficial components that are in oxalate-containing foods such as alkali, magnesium, phytate and fiber.23 Noori et al. found urinary magnesium, citrate and pH increased in patients without SBS following a DASH (Dietary Approaches to Stop Hypertension) style diet compared to a low oxalate diet.24 Siener et al. found that by providing meals that were “balanced” with less oxalate, protein and sodium, along with more fiber and magnesium, patients with SBS had reduced urine oxalate.25 Finally, Bianco et al. found that advice to reduce dietary oxalate given in the clinic did not lower urine oxalate in a group of patients with SBS.22 As such, a strict low oxalate diet for patients with SBS should also be questioned. 

Although avoidance of eating foods that are very high in oxalate is prudent for patients with enteric hyperoxaluria, a strict low oxalate diet should not be recommended as it will limit beneficial components for stone prevention and general health.23,24 Also, it is hard for patients to adhere to a  prescribed amount of dietary oxalate given the difficulty of quantifying oxalate in food (especially prepackaged foods), incomplete lists of oxalate content of foods, discrepancies between lists of food oxalate composition, and the prevalence of misinformation.25 In addition, oxalate exists in both soluble and insoluble forms; soluble oxalate has a much larger impact on urine oxalate levels, yet this distinction is not usually made on food composition lists.27 Table 4 provides a short list of foods with moderate and high oxalate concentration (>70 mg oxalate per standard portion as measured by the 2023 Harvard Oxalate Table).28 Practically, ensuring adequate dietary calcium is a more effective and healthy way to reduce urine oxalate.

Table 4. Very High Oxalate Foods & Substitutes29

Food ItemOxalate (mg)Lower Oxalate SubstitutionsOxalate (mg)
Spinach, ½ cup cooked547Kale, ½ cup cooked1
Navy beans, ½ cup cooked96Kidney beans, ½ cup cooked10
White potato with skin, 1 medium92Mashed or boiled potatoes, 1 cup30
Beets, ½ cup cooked76Parsnip, ½ cup cooked15
Almonds, 1 ounce (1/4 cup)72Pistachios, 1 ounce, ¼ cup9

Bile acid sequestrants, such as cholestyramine, are also used to bind oxalate in the SB and reduce urine oxalate.29,30 However, the use of bile acid sequestrants can lead to bile salt deficiency which will worsen fat malabsorption, hence increasing risk of oxalate absorption. Therefore, in patients with SBS it is necessary to provide clinical monitoring of the effectiveness of a bile salt sequestrant to determine if the resin improves or worsens a patient’s malabsorption.

Correction of Hypomagnesemia

Given the prevalence of hypomagnesemia, and the role that magnesium plays in oxalate stone prevention, the correction of hypomagnesemia may help prevent oxalate stones. Foods highest in magnesium include nuts, seeds, beans, and green leafy vegetables. Unfortunately, these foods may not be tolerated by some patients with SBS. In addition, dietary magnesium is unlikely to significantly raise serum magnesium levels in SBS patients with limited absorptive capacity and oral magnesium supplements may worsen stool output and dehydration. Therefore, parenteral magnesium replacement may be necessary to raise urinary magnesium levels and reduce stone formation.5

“Do No Harm”

Given the high risk of malnutrition, maldigestion, and malabsorption in patients with SBS, it is imperative that nutrition recommendations do not become so onerous that they make it more difficult for patients with SBS to balance their diet. Restrictive diets have been shown to reduce total calorie intake in frail populations.31 Ideally, nutrition recommendations should be devised, communicated and monitored by a registered dietitian to optimize patient adherence and prevent malnutrition.

Summary

Short bowel syndrome significantly increases the risk of kidney stone formation due to a combination of possible factors including reduced urine volume, magnesium, citrate, pH and increased oxalate. Kidney stone prevention interventions should be personalized to 24-hour urine collection results and patient preferences. A comprehensive nutrition assessment should be completed prior to providing dietary recommendations given the high risk of malnutrition. All patients with SBS that have or are at risk for kidney stone formation should be followed by a team that is knowledgeable in the prevention and management of kidney stones.

References

1. Nightingale JM, Lennard-Jones JE, Gertner DJ, Wood SR, Bartram CI. Colonic preservation reduces need for parenteral therapy, increases incidence of renal stones, but does not change high prevalence of gall stones in patients with a short bowel. Gut. 1992;33(11):1493-1497.
2. Teichman JMH. Acute Renal Colic from Ureteral Calculus | NEJM. New England Journal of Medicine. 2004;350:684-693.
3. Pironi L. Definition, classification, and causes of short bowel syndrome. Nutr Clin Pract. 2023;38 Suppl 1:S9-S16.
4. Matarese LE, O’Keefe SJ, Kandil HM, Bond G, Costa G, Abu-Elmagd K. Short Bowel Syndrome: Clinical Guidelines for Nutrition Management. Nutrition in Clinical Practice. 2005;20(5):493-502.
5. Bering J, DiBaise JK. Short bowel syndrome: Complications and management. Nutrition in Clinical Practice. 2023;38(S1):S46-S58.
6. Chewcharat A, Curhan G. Trends in the prevalence of kidney stones in the United States from 2007 to 2016. Urolithiasis. 2021;49(1):27-39.
7. Wang P, Yang J, Zhang Y, Zhang L, Gao X, Wang X. Risk Factors for Renal Impairment in Adult Patients With Short Bowel Syndrome. Front Nutr. 2021;7.
8. Deren JJ, Porush JG, Levitt MF, Khilnani MT. Nephrolithiasis as a complication of ulcerative colitis and regional enteritis. Ann Intern Med. 1962;56:843-853.
9. Maratka Z, Nedbal J. Urolithiasis as a complication of the surgical treatment of ulcerative colitis. Gut. 1964;5(3):214-217.
10. Worcester EM. Stones from bowel disease. Endocrinol Metab Clin North Am. 2002;31(4):979-999.
11. Pearle MS, Goldfarb DS, Assimos DG, et al. Medical Management of Kidey Stones: AUA Guideline. J Urol. 2014;192:316-324.
12. Haghighatdoost F, Sadeghian R, Clark CCT, Abbasi B. Higher Dietary Acid Load Is Associated With an Increased Risk of Calcium Oxalate Kidney Stones. Journal of Renal Nutrition. 2021;31(5):467-474.
13. Holmes RP, Goodman HO, Assimos DG. Contribution of dietary oxalate to urinary oxalate excretion. Kidney International. 2001;59(1):270-276.
14. Borghi L, Schianchi T, Meschi T, et al. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med. 2002;346(2):77-84.
15. Witting C, Langman CB, Assimos D, et al. Pathophysiology and Treatment of Enteric Hyperoxaluria. CJASN. 2021;16(3):487-495.
16. Wu J, Yang Z, Wei J, Zeng C, Wang Y, Yang T. Association Between Serum Magnesium and the Prevalence of Kidney Stones: a Cross-sectional Study. Biol Trace Elem Res. 2020;195(1):20-26.
17. Deshmukh SR, Khan ZH. Evaluation of urinary abnormalities in nephrolithiasis patients from Marathwada region. Indian J Clin Biochem. 2006;21(1):177-180.
18. Taheri M, Jalali S, Borumandnia N, Tavasoli S, Basiri A, Taheri F. Effect of magnesium oxide or citrate supplements on metabolic risk factors in kidney stone formers with idiopathic hyperoxaluria: a randomized clinical trial. Magnes Res. 2024;37(1):12-21.
19. Galán-Llopis JA, Sánchez-Pellicer P, Navarro-López V. Role of microbiome in kidney stone disease. Current Opinion in Urology. 2023;33(2):84-89.
20. Johnson E, Vu L, Matarese LE. Bacteria, Bones, and Stones: Managing Complications of Short Bowel Syndrome. Nutr Clin Pract. 2018;33(4):454-466.
21. Bianco J, Chu F, Bergsland K, Coe F, Worcester E, Prochaska M. What treatments reduce kidney stone risk in patients with bowel disease? Urolithiasis. 2022;50(5):557-565.
22. Curhan GC, Willett WC, Speizer FE, Spiegelman D, Stampfer MJ. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Intern Med. 1997;126(7):497-504.
23. Penniston KL. Is It Time to Retire the Low-Oxalate Diet? Yes. J Endourol. 2021;35(10):1431-1434.
24. Noori N, Honarkar E, Goldfarb DS, et al. Urinary Lithogenic Risk Profile in Recurrent Stone Formers With Hyperoxaluria: A Randomized Controlled Trial Comparing DASH (Dietary Approaches to Stop Hypertension)-Style and Low-Oxalate Diets. American Journal of Kidney Diseases. 2014;63(3):456-463.
25. Siener R, Ernsten C, Welchowski T, Hesse A. Metabolic Profile of Calcium Oxalate Stone Patients with Enteric Hyperoxaluria and Impact of Dietary Intervention. Nutrients. 2024;16(16):2688.
26. Attalla K, De S, Monga M. Oxalate Content of Food: A Tangled Web. Urology. 2014;84(3):555-560.
27. Ritter MMC, Savage GP. Soluble and insoluble oxalate content of nuts. Journal of Food Composition and Analysis. 2007;20(3):169-174.
28. Harvard T. H Chan School of Public Health. Oxalate Table. Published online November 2023. Accessed September 30, 2024. https://www.hsph.harvard.edu/nutrition-questionnaire-service-center/wp-content/uploads/sites/2637/2023/11/OXALATE-TABLE-1.xlsx
29. Kapral C, Wewalka F, Praxmarer V, Lenz K, Hofmann AF. Conjugated bile acid replacement therapy in short bowel syndrome patients with a residual colon. Z Gastroenterol. 2004;42(7):583-589.
30. Emmett M, Guirl MJ, Santa Ana CA, et al. Conjugated bile acid replacement therapy reduces urinary oxalate excretion in short bowel syndrome. Am J Kidney Dis. 2003;41(1):230-237.

Download Tables, Images & References

From the Pediatric Literature

Intestinal Ultrasound Use in Pediatric IBD

Pediatric inflammatory bowel disease (IBD) in children requires endoscopic intervention for initial diagnosis and for continued disease surveillance. Intestinal ultrasound (IU) has the potential to be less invasive while also accurate when used as a diagnostic modality for IBD. The authors of this study evaluated IU in comparison to pediatric endoscopy and fecal calprotectin testing in the diagnosis of pediatric IBD via a prospective study performed over one year.

Pediatric patients (age 2-21 years) who had previously undergone colonoscopy (including terminal ileum intubation) were divided into 2 groups consisting of patients with IBD and patients without IBD. A subsequent IU occurred one month after colonoscopy, and five segments of the intestine were evaluated (terminal ileum, ascending colon, transverse colon, descending colon, and rectum).  IU studies were read by three pediatric radiologists, and all radiologists and gastroenterologists involved in the study were blinded to each other’s findings. IU documentation included bowel wall thickness, hyperemia, presence of fatty proliferation, and absence of wall stratification. A modified ultrasound-ulcerative colitis index was used as a scoring system to determine bowel wall inflammation, and bowel wall thickness was scored based on millimeter thickness. For example, a score of “0” was given for normal thickness; “1” was given for a thickness of 3 to 5 millimeters; “2” was given for a thickness of 5 to 7 millimeters; and “3” was given for a thickness greater than 7 millimeters. The presence of hyperemia, fatty proliferation, and absence of wall stratification were each given a score of “1” if present. A Mayo score was used to document endoscopic colon inflammation for ulcerative colitis while a Simple Endoscopic Score for Crohn Disease (SES-CD) was used to determine endoscopic colon inflammation for Crohn disease. Individual patient data including assessments for disease activity were collected.  Disease activity was assessed by fecal calprotectin level, the Pediatric Ulcerative Colitis Activity Index (PUCAI), and the Pediatric Crohn Disease Activity Index (PCDAI).

In total, 50 patients were included in the study (median age 13.5 years; 58% female). Half of these patients were diagnosed with IBD in which 12 patients had ulcerative colitis, 12 patients had Crohn disease, and 1 patient had IBD unclassified. The other 25 patients had no IBD, and there was no difference in age distribution between these two groups. Patients with ulcerative colitis had a median PUCAI of 52.5 and a Mayo score of 8.5. Patients with Crohn disease had a median PCDAI of 42.5 and a SES-CD of 16.5. IU demonstrated bowel wall thickness in 23 patients (46%) for which 19 of these patients had IBD (82.6%). A bowel inflammation score of at least “1” was associated with 76% sensitivity, 84% specificity, 83% positive predictive value (PPV), 78% negative predictive value (NPV), and a Pearson’s chi-square being <0.001when patient with IBD were compared to patients without IBD.

Sensitivity, specificity, PPV, and NPV improved further if only moderate or severe endoscopic disease was included. Pearson correlation coefficient testing demonstrated a significant correlation between IU scoring and fecal calprotectin levels as well as IU and endoscopic scoring (Mayo score and SES-CD). No such correlation existed between IU and clinical scoring (PUCAI and PCDAI).

IU appears to have potential utility in the diagnosis of pediatric IBD, especially since this study noted good correlation with fecal calprotectin levels and endoscopic scoring systems. It also may prove to be a good non-interventional testing technique to follow up on disease activity after a diagnosis of IBD is made in a child.

Khan H, Munden M, Spence L, Jones R, Whatley J, Suppa C. Intestinal ultrasound at diagnosis of pediatric inflammatory bowel disease compared to endoscopy. Journal of Pediatric Gastroenterology and Nutrition. 2024; doi: 10.1002/jpn3.12444.\Online ahead of print.

More Data on Exclusive Enteral Nutrition as Treatment for Crohn Disease in Children

One potential therapy for some cases of Crohn disease in children is exclusive enteral nutrition (EEN). Although EEN can be effective in the treatment of Crohn disease, its associated dietary limitations potentially can lead to eating disorders. The authors of this study determined the risk of eating disorder development in the setting of EEN therapy for pediatric Crohn disease. This retrospective study occurred over a four-month period at a children’s hospital in Paris, France. A questionnaire was developed which covered basic patient information, EEN use (including duration and how it was administered), potential difficulties with EEN use, follow-up data, long-term risks, and patient opinion on EEN therapy.

Out of the 450 pediatric patients with Crohn disease that were evaluated, 92 patients (20%) were receiving EEN and only 32 patients (7%) completed the survey. Survey respondents were 32% female, and most patients (84%) were 10 years of age or older. Ileocolonic disease was present in 50% of patients, and 75% of patients had non-stricturing/non-penetrating disease. Normal growth was present in 84% of patients. All patients who completed the survey had at least one eating difficulty associated with EEN for which the main difficulty was loss of eating desire. Enteral therapy discontinuation occurred in 12 patients receiving EEN (38%) for which the primary cause was intolerance of EEN treatment. Gastrointestinal symptom continuation was present in 8 patients (25%). The average time for patients to have an improvement while on EEN was 6 weeks, and most patients (62%) received continuing support from a multidisciplinary healthcare team.

Persistent eating difficulties remained in 10 patients (32%) after a median of 5 years post EEN, and patients receiving behavioral therapy during EEN did not develop long-term feeding issues. It was noted that 19 patients (59%) recommended use of EEN as treatment for Crohn disease mainly because it avoided use of medication.

This small study demonstrated that although EEN was effective and tolerable for many pediatric patients with Crohn disease, a sizable group of patients did not tolerate EEN and had persistence of eating difficulties long after EEN had been stopped. These findings suggest that psychological therapy is essential during EEN for pediatric Crohn disease, and frequent screening for the development of possible eating disorders during EEN is required.

Sandrine C, Emmanuelle D, Jerome V, Christine M. Exclusive enteral nutrition for induction of remission in pediatric Crohn＊s disease: short- and long-term tolerance and acceptance. JPGN Reports. 2024; https://doi.org/10.1002/jpr3.12163. Online ahead of print.

Constipation in Children with Inflammatory Bowel Disease

Children with inflammatory bowel disease (IBD) typically present with abdominal pain, blood in the stool, diarrhea, and weight loss. However, such children also can have constipation which can delay a diagnosis of IBD. Since the worldwide prevalence of pediatric functional constipation (FC) may be as high as 29.6%, it is imperative to be able to delineate children with sole FC from patients with FC and organic gastrointestinal disease. The authors of this Italian study attempted to determine the prevalence of constipation in children who eventually were diagnosed with IBD.

This study was retrospective, observational, and cross-sectional in which children diagnosed with either Crohn disease or ulcerative colitis over an 8-year period were reviewed. Initial patient characteristics were obtained, including IBD symptom duration, disease location (per the Paris Classification), the Pediatric Crohn’s Disease Activity Index (PCDAI) score, the Pediatric Ulcerative Colitis Activity Index (PUCAI) score, the Ulcerative Colitis Endoscopic Index of Severity (UCEIS) score, and the Simplified Endoscopic Score for Crohn disease (SES-CD) score. Patients with IBD who also had FC based on Rome IV Criteria at the initial follow-up clinic visit or phone call were included in the study.

Full data regarding a patient’s IBD diagnosis was present in 238 patients for which 104 patients (44%) had Crohn disease, 130 patients (56%) had ulcerative colitis, and 4 patients (0.016%) had IBD Unclassified. The mean age of patients was 174 ± 47 months, and 53% of these patients were male. A total of 41 of all patients with IBD met Rome IV criteria for FC. The authors noted that 18.2% of patients with Crohn disease, 21.5% of patients with ulcerative colitis, and none of these patients with IBD Unclassified had FC. None of the patients with IBD and FC had other autoimmune diseases, and there was no statistical difference in age, gender, extra-intestinal manifestations of IBD, age at IBD diagnosis, surgery, use of induction therapy, and IBD relapse when patients with IBD with FC were compared to patients with IBD and no FC. However, patients with IBD and FC were statistically more likely to have a delay in IBD diagnosis. Patients with IBD and no FC were statistically more likely to have diarrhea or bloody diarrhea. Initial PUCAI scoring also was statistically higher for patients with ulcerative colitis and no FC. Patients with Crohn disease and FC were statistically more likely to have perianal disease changes. Patients with ulcerative colitis and FC were statistically more likely to have proctitis and left-sided colitis. Serum testing and stool testing, including fecal calprotectin levels, were similar between patients with IBD with or without FC.

Laxatives were used in 69% of patients prior to an IBD diagnosis in patients with IBD and FC with 65% of these patients receiving PEG3350 medication. A statistically significant higher serum erythrocyte sedimentation rate (ESR) level was present in patients with IBD and FC who had not received PEG3350. Interestingly, there was a statistically significant delay in IBD diagnosis in patients with IBD and FC who did not receive PEG3350 therapy.

This study demonstrates that FC can occur in a sizable percentage of children with IBD. If a child with FC is not improving on laxative therapy, further testing, including a good anal/rectal examination and possible endoscopy is warranted.

Sabrina C, Antonio C, Salomone S, Daniela P, Marianna C, Pietro B, Massimo M, Erasmo M, Annamaria S, Caterina S. The prevalence of constipation in children with new diagnosis of inflammatory bowel disease (IBD): a retrospective study.  Journal of Pediatric Gastroenterology and Nutrition 2025; doi: 10.1002/jpn3.70005.\Online ahead of print.

PFAPA Outcomes in Children

Periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis syndrome (PFAPA) affects children and typically is associated with recurring fevers, stomatitis, pharyngitis, and cervical adenitis. Pediatric gastroenterologists often see such patients as children with PFAPA also can have associated abdominal pain, emesis, and diarrhea. Although the cause of PFAPA is unknown, tonsillectomy seems to be effective in relieving PFAPA symptoms.  The authors of this study evaluated the long-term symptoms of PFAPA after tonsillectomy.

This retrospective study occurred over a 14-year period and included all patients who had been diagnosed with PFAPA and also who had undergone a subsequent tonsillectomy. All patients with PFAPA met the Marshall criteria for this disorder.  Patients who met inclusion criteria initially were contacted by mail or by phone and subsequently had data collected by phone interview. Initial symptoms prior to tonsillectomy were obtained by medical record review. Included patients and their families were queried regarding the presence of fever (defined as temperature greater than 380 Celsius) as well as the persistence of any other symptoms associated with PFAPA after tonsillectomy. Patients were divided into 4 groups: symptom resolution, persistence of PFAPA-symptoms but no fever, less/milder febrile episodes, or no clinical change.

A total of 101 patients had data available for which 82 patients participated in the study. The median patient age at the time of interview was 14.8 years (range 6 – 28.8 years). The median age of developing PFAPA symptoms was 1.8 years (range 0.1 – 16 years). The median age of tonsillectomy was 5.1 years (range 2.3 – 18.8 years). Five patients had undergone genetic testing for periodic fever syndromes in the setting of PFAPA, but no associated genetic syndromes were detected. Median long term follow-up time after tonsillectomy was 8.8 years (range 2.8 – 16.1 years). It should be noted that gastrointestinal symptoms prior to tonsillectomy included abdominal pain (35% of patients) and nausea and emesis (16% of patients).

Resolution of fever episodes 6 months after tonsillectomy occurred in 52% of patients. Persistence of non-febrile PFAPA symptoms 6 months after tonsillectomy was present in 22% of patients.The most common non-febrile PFAPA symptoms were low-grade fever, malaise, aphthous ulcers, pharyngitis, cervical adenitis, arthralgias, abdominal pain, and headache. Persistence of less/milder febrile episodes was present in 20% of patients 6 months post tonsillectomy while 1% of patients had no clinical change 6 months post tonsillectomy. Children with PFAPA symptom resolution at 6 months post tonsillectomy were significantly more likely to maintain symptoms response long term compared to those patients with a partial response 6 months post tonsillectomy. Long-term data demonstrated that 89% of patients who had initial symptom resolution post tonsillectomy still maintained symptom resolution. It was noted that 26% of patients with initial persistence of non-febrile PFAPA symptoms still had associated symptoms. Also, 35% of patients with initial less/milder febrile episodes still had symptoms. Long-term gastrointestinal symptoms after tonsillectomy consisted of abdominal pain (40%) and nausea and emesis (33%) in patients with persistent fever symptoms as well as abdominal pain (12%) and nausea and emesis (29%) in patients with non-febrile symptoms.

This study demonstrates that tonsillectomy can ameliorate periodic fever in most pediatric patients with PFAPA. However, non-febrile symptoms can continue long term, even after tonsillectomy. Such symptoms can be gastrointestinal in nature, and it is imperative to make sure non-PFAPA conditions, such as inflammatory bowel disease, are not occurring in this patient population.

Moberg T, Rydenman K, Berg S, Fasth A, Wekell P. Long-term symptoms in periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis syndrome after tonsillectomy.  Journal of Pediatrics; 2025: 114424.

Download Tables, Images & References

FRONTIERS IN ENDOSCOPY, SERIES #93

Ablation of the Gastric Cardia for GERD: A Comprehensive Technical and Clinical Review

May 2025 • Volume XLIX, Issue 5
Sheza Malik,Douglas G. Adler

Read Article

Anti-Reflux Mucosal Ablation (ARMA) is an innovative endoscopic intervention for managing PPI-refractory GERD by enhancing the structural integrity of the gastroesophageal junction (GEJ). Utilizing controlled thermal ablation, ARMA induces localized mucosal fibrosis to reinforce the anti-reflux barrier. Clinical studies demonstrate significant improvements in GERD symptoms, acid exposure time, and DeMeester scores, with over 70% clinical success in one year. The procedure is well-tolerated, with manageable complications such as transient stenosis treated via endoscopic dilation. ARMA offers advantages over surgical fundoplication due to its reduced procedural complexity and minimally invasive nature. While early outcomes are promising, larger multicenter trials are needed to validate long-term efficacy and define optimal patient selection, particularly in those with mild to moderate GEJ abnormalities.

Introduction

Gastroesophageal reflux disease (GERD) is a highly prevalent condition. GERD is characterized by the retrograde movement of gastric contents into the esophagus, leading to symptoms such as heartburn, regurgitation, and atypical presentations like cough, chest pain, hoarseness, and laryngitis. GERD affects an estimated 20% of adults in Western populations and incurs significant healthcare costs while impairing quality of life.1,2

Despite the widespread use of proton pump inhibitors (PPIs) as the first-line therapy, 30–40% of patients continue to experience symptoms despite adequate acid suppression.3,4 Surgical interventions such as laparoscopic Nissen fundoplication are highly effective but are associated with complications like dysphagia and gas bloat syndrome and have a significant failure rate, necessitating the exploration of less invasive alternatives.5,6,7

Anti-reflux mucosal interventions, including Anti-Reflux Mucosectomy (ARMS) and Anti-Reflux Mucosal Ablation (ARMA), have emerged as innovative endoscopic procedures aimed at improving the anatomical and functional integrity of the gastroesophageal junction (GEJ). These techniques are gaining traction as viable options for managing PPI-refractory GERD.8 This article will review the current status of ARMS and ARMA. 

Pathophysiology of GERD and Role of the GEJ

The pathogenesis of GERD is multifactorial, involving structural and functional abnormalities of the GEJ.9 Key contributors include:

Impaired Lower Esophageal Sphincter (LES) Pressure: A hypotensive LES facilitates retrograde reflux.10

Hiatal Hernia: Alters the anatomical configuration of the GEJ and diaphragm, reducing its anti-reflux competency, and allowing acid-producing gastric mucosa above the diaphragm.11

Transient LES Relaxations (TLESRs): Excessive, non-swallowing LES relaxations increase reflux events.12

Esophageal Clearance Dysfunction: Impaired peristalsis delays the clearance of refluxed material.13

Hill’s classification (grades I–IV) of the gastroesophageal flap valve provides a structural assessment of the GEJ, with grades II-IV associated with an increased risk of PPI-refractory GERD.1,7 Endoscopic therapies like ARMA directly target the structural deficiencies of the GEJ, offering a minimally invasive alternative to surgical fundoplication 

Evolution of Endoscopic Therapies

Endoscopic approaches to GERD management have advanced significantly, offering effective alternatives to traditional medical and surgical treatments.14  These approaches can be categorized into several techniques, as shown in Table 1.

1. Reconstructive Therapies:

○ Transoral Incisionless Fundoplication (TIF):Creates full-thickness plications to mimic surgical fundoplication. While effective, it is technically demanding, time-consuming, and requires specialized training and equipment.15

○ Magnetic Sphincter Augmentation (LINX): Places a ring of magnetic beads around the LES via laparoscopy. It has shown promise but is limited by MRI incompatibility, specific anatomical requirements, and risk of adverse events including dysphagia and device breakage, among others.16

2. Ablative Therapies:

○ Radiofrequency Ablation (RFA): Remodels LES muscle fibers using devices like Stretta but has variable efficacy.17

○ ARMS: Involves partial mucosal resection at the gastric cardia to induce scar-mediated tightening of the GEJ.8

○ ARMA: Focuses on controlled thermal ablation of the gastric cardia mucosa, leading to scar formation and enhanced flap valve integrity.8

Technical Considerations of ARMA

ARMA is a minimally invasive endoscopic procedure aimed at reinforcing the GEJ by inducing targeted mucosal scarring to enhance the anti-reflux barrier.18

The procedure begins with the patient positioned in the left lateral decubitus position. General anesthesia is typically used to ensure patient comfort and procedural safety, although conscious sedation may suffice in select cases based on the patient’s clinical status and tolerance. A high-definition gastroscope fitted with a transparent hood enhances visualization and precision. Ablation zones are marked in a butterfly-shaped pattern along the gastric side of the cardia, leaving two non-ablated segments to avoid circumferential scarring and mitigate the risk of stenosis. This pattern is crucial for ensuring localized scar formation without excessive narrowing of the lumen. Submucosal injection of saline mixed with indigo carmine dye is performed to lift the mucosa and create a protective cushion, safeguarding deeper layers from thermal injury during ablation.17,18

Table 1. Comparative Analysis of Endoscopic Therapies for GERD

Therapy Mechanism of Action Ideal Patient Profile Advantages Challenges and Limitations 
Transoral Incisionless Fundoplication (TIF) Uses polypropylene fasteners to create full-thickness plications at the GEJ, replicating a partial fundoplication – PPI-refractory GERD with Hill grade II/III  – Hiatal hernia ≤2 cm  – Normal esophageal motility – Mimics surgical fundoplication  – Avoids surgical incisions  – Reduces regurgitation and improves LES function – Requires specialized equipment and technical expertise  – Limited by anatomical constraints (e.g., large hiatal hernias)  – Recurrence rates in patients with anatomical defects 
Radiofrequency Ablation (RFA) Delivers radiofrequency energy to the LES, inducing controlled fibrosis and hypertrophy – PPI-dependent GERD  – Hypotensive LES without major anatomical defects – Outpatient procedure  – Minimal invasiveness  – No need for general anesthesia – Variable outcomes in symptom relief  – Limited data on long-term efficacy  – Less effective in patients with severe reflux or large hiatal hernias 
Anti-Reflux Mucosectomy (ARMS) Partial mucosal resection at the gastric cardia induces scar formation, creating a tighter GEJ – PPI-refractory GERD with Hill grade II/III  – GERD post-bariatric surgery  – Moderate anatomical abnormalities – Demonstrated efficacy in PPI-refractory cases  – Improves acid exposure and esophagitis  – Enhances flap valve mechanism – Higher technical difficulty  – Increased risk of perforation and post-procedural strictures  – Requires expertise in endoscopic mucosal resection 
Anti-Reflux Mucosal Ablation (ARMA) Controlled thermal ablation of gastric cardia mucosa induces contraction and scarring to strengthen the GEJ – PPI-refractory GERD with Hill grade II/III  – Small (<3 cm) hiatal hernia  – Normal or mildly impaired LES tone – Safe and reproducible technique  – Lower complication rates compared to ARMS  – Effective in symptom relief and acid control – Limited long-term follow-up data  – Risk of transient stenosis (13.2%) treated with endoscopic dilation  – Unsuitable for severe anatomical defects 
Antireflux Mucosal Valvuloplasty (ARMV) Combines mucosal resection with flap reconstruction to mimic natural anti-reflux barriers – GERD with moderate anatomical GEJ disruption  – Patients intolerant to long-term PPI use – Innovative dual mechanism (scar contraction + mucosal flap)  – Potentially superior anatomical restoration – Experimental stage  – Limited data from randomized controlled trials  – Requires advanced endoscopic skills 
Magnetic Sphincter Augmentation (LINX®) Places a magnetic ring around the LES to enhance closure and reduce reflux – PPI-refractory GERD without major anatomical abnormalities  – Small (<2 cm) hiatal hernia – Outpatient or short-stay procedure  – Preserves normal swallowing and belching mechanisms – Incompatible with MRI  – Device erosion and migration risks  – High costs and limited long-term outcome data 

 Mucosal ablation is typically conducted using electrocautery in spray coagulation mode. The generator settings commonly used for electrocautery include effect 2 and 50 W power, which deliver controlled thermal energy for uniform ablation. In some studies, argon plasma coagulation (APC) has been employed as an alternative, providing effective mucosal ablation while reducing the risk of deep thermal injury. When APC is used, the same generator settings are often applied to ensure consistent outcomes. While radiofrequency ablation (RFA) devices may be considered, APC remains the preferred method based on safety, availability, and efficacy data in the literature.18,21 (Figure 1)

A crucial patient selection criterion is the presence and size of a hiatal hernia. ARMA is most effective in patients with small hernias (<2 cm). Larger hernias (>2 cm) typically require surgical repair, as ARMA does not address the anatomical displacement of the GEJ associated with larger hernias. Thus, a pre-procedure assessment, including endoscopy and esophageal manometry, is essential.  Post-procedurally, patients are prescribed PPI therapy for 4 – 6 weeks to promote mucosal healing, minimize inflammation, and reduce the risk of complications such as ulcers or delayed bleeding. Follow-up includes reassessment of symptoms using validated GERD questionnaires, endoscopic examination, and, if indicated, 24-hour pH monitoring.18

Clinical Outcomes

ARMA has shown significant efficacy in improving GERD-related symptoms and objective reflux control. A 2024 international bi-center study reported a reduction in median GERD-HRQL scores from 26 to 11 at six months (P < 0.001), Acid Exposure Time (AET) fell from 5.3% to 0.7% (P = 0.003), alongside significant improvements in DeMeester scores. Follow-up data at 12 months indicated a clinical success rate of 70%, defined as a greater than 50% reduction in validated GERD questionnaire scores, suggesting durable symptomatic and reflux improvements over time.23

A meta-analysis of 15 nonrandomized studies (n = 461) demonstrated a technical success rate of 100% and clinical success rates of 78% at six months, 72% at one year, and 73% at three years, with consistent outcomes across ARMS and ARMA. At one year, 64% of patients were off PPIs, with significant improvements observed in symptom scores, esophagitis resolution, and acid exposure time (P < 0.01). These findings underscore ARMA’s ability to potentially deliver durable symptom relief and effective reflux control, offering a promising therapeutic option for refractory GERD.8

Safety and Adverse Events

The safety profile of ARMA, while promising, reflects the early stages of adoption and ongoing evaluation of this emerging technology. In clinical studies, transient stenosis was observed in 13.2% of cases, all of which were effectively managed with endoscopic balloon dilation. Other adverse events included minor bleeding and mucosal ulceration, both of which resolved with conservative management, including short-term PPI therapy. Importantly, no perforations or severe adverse events, such as significant bleeding requiring transfusion or long-term complications, were reported in the available data. These findings highlight the need for ongoing studies to validate the long-term safety and risk profile of ARMA while acknowledging its manageable short-term complications.23,24

Comparative Effectiveness of ARMA

Compared to ARMS and other endoscopic therapies, ARMA offers distinct clinical advantages. Its controlled thermal ablation approach avoids full-thickness mucosal resection, resulting in lower technical complexity, significantly shorter procedure times, and a reduced risk of perforation. This makes ARMA more accessible and less invasive for a broader range of patients. The procedure is particularly effective in patients with prior gastric cardia fibrosis (e.g., due to previous interventions or inflammation) or anatomical modifications, such as post-bariatric surgery anatomy or hiatal hernias smaller than 2 cm, thereby broadening its applicability.17, 21

In a randomized trial comparing ARMA to PPI therapy, ARMA demonstrated superior symptom control, improved mucosal integrity, and significant reductions in acid reflux parameters, including acid exposure time and DeMeester scores. These findings support its role as an effective treatment for GERD refractory to pharmacological therapy. While short-term PPI therapy (approximately 4 – 6 weeks) is typically recommended post-procedure to promote mucosal healing, many patients experience reduced long-term dependence on PPIs due to the durable improvements provided by ARMA.

Limitations and Future Directions

While ARMA has shown promising short-term outcomes, several limitations remain. Most studies provide data for up to 12 months, leaving long-term durability uncertain. Additionally, the majority of evidence comes from single-center and small-scale trials, necessitating larger, multicenter randomized controlled trials to validate findings. Current studies also focus primarily on PPI-refractory GERD in patients with mild to moderate anatomical abnormalities, limiting generalizability. Future research should explore ARMA’s long-term durability, comparative efficacy with surgical fundoplication, emerging endoscopic techniques such as antireflux mucosal valvuloplasty (ARMV), and its cost-effectiveness in routine clinical practice.27 Optimization of patient selection criteria, particularly anatomical and functional predictors of success, is crucial to further refine its role in GERD management.25

Conclusion

ARMA is a novel endoscopic technique that is promising in the minimally invasive management of GERD. By targeting the gastroesophageal junction (GEJ) to enhance its structural integrity, ARMA has demonstrated effectiveness in reducing GERD symptoms, particularly in patients with PPI-refractory disease. However, as a relatively new intervention, its long-term efficacy and safety profile require further validation through robust, multicenter studies. While early evidence suggests ARMA may serve as a valuable addition to the therapeutic arsenal for GERD, its role relative to established medical and surgical treatments will be further defined as additional studies and data emerge. 

References

References
1. Nirwan, J.S., Hasan, S.S., Babar, ZUD. et al. Global
Prevalence and Risk Factors of Gastro-oesophageal Reflux
Disease (GORD): Systematic Review with Meta-analysis. Sci
Rep 10, 5814 (2020).
2. Revicki DA, Wood M, Maton PN, Sorensen S. The impact of
gastroesophageal reflux disease on health-related quality of
life. Am J Med. 1998;104(3):252-258.
3. Sandhu DS, Fass R. Current Trends in the Management of
Gastroesophageal Reflux Disease. Gut Liver. 2018;12(1):7-16.
4. Heading RC. Proton pump inhibitor failure in gastro-oesophageal
reflux disease: a perspective aided by the Gartner hype
cycle. Clin Med (Lond). 2017;17(2):132-136.
5. Sato K, Awad ZT, Filipi CJ, et al. Causes of long-term
dysphagia after laparoscopic Nissen fundoplication. JSLS.
2002;6(1):35-40.
6. Salinas J, Georgiev T, González-Sánchez JA, López-Ruiz
E, Rodríguez-Montes JA. Gastric necrosis: A late complication
of nissen fundoplication. World J Gastrointest Surg.
2014;6(9):183-186.
7. Hunter JG, Smith CD, Branum GD, et al. Laparoscopic fundoplication
failures: patterns of failure and response to fundoplication
revision. Ann Surg. 1999;230(4):595-606.
8. Rodríguez de Santiago E, Sanchez-Vegazo CT, Peñas B, et
al. Antireflux mucosectomy (ARMS) and antireflux mucosal
ablation (ARMA) for gastroesophageal reflux disease:
a systematic review and meta-analysis. Endosc Int Open.
2021;9(11):E1740-E1751. Published 2021 Nov 12.
9. Odze RD. Pathology of the gastroesophageal junction. Semin
Diagn Pathol. 2005;22(4):256-265.
10. Sidhu AS, Triadafilopoulos G. Neuro-regulation of lower
esophageal sphincter function as treatment for gastroesophageal
reflux disease. World J Gastroenterol. 2008;14(7):985-
990.
11. Hyun JJ, Bak YT. Clinical significance of hiatal hernia. Gut
Liver. 2011;5(3):267-277.
12. Iwakiri K, Hayashi Y, Kotoyori M, et al. Transient lower
esophageal sphincter relaxations (TLESRs) are the major
mechanism of gastroesophageal reflux but are not the cause of
reflux disease. Dig Dis Sci. 2005;50(6):1072-1077.
13. Simrén M, Silny J, Holloway R, Tack J, Janssens J, Sifrim D.
Relevance of ineffective oesophageal motility during oesophageal
acid clearance. Gut. 2003;52(6):784-790.
14. Hopkins J, Switzer N J, Karmali S. Update on novel endoscopic
therapies to treat gastroesophageal reflux disease: A
review. World J Gastrointest Endosc. 2015;7:1039–1044. doi:
15. Ihde GM. The evolution of TIF: transoral incisionless fundoplication.
Therap Adv Gastroenterol. 2020;13:1756284820924206.
Published 2020 May 21.
16. Cammarata F, Novia M, Aiolfi A, et al. Magnetic Sphincter
Augmentation for Gastroesophageal Reflux After
Sleeve Gastrectomy: A Systematic Review. Obes Surg.
2024;34(11):4232-4243.
17. Pandolfino JE. The Use of Endoscopy and Radiofrequency
Ablation for the Treatment of GERD. Gastroenterol Hepatol
(N Y). 2015;11(12):847-849.
18. Inoue H, Tanabe M, de Santiago ER, et al. Anti-reflux mucosal
ablation (ARMA) as a new treatment for gastroesophageal
reflux refractory to proton pump inhibitors: a pilot study.
Endosc Int Open. 2020;8(2):E133-E138.
19. Lopes SO, Gonçalves AR, Macedo G, Santos-Antunes J.
Endoscopic treatment of gastroesophageal reflux: a narrative
review. Porto Biomed J. 2023;8(4):e226. Published 2023 Aug
3.
20. Pandolfino JE. The Use of Endoscopy and Radiofrequency
Ablation for the Treatment of GERD. Gastroenterol Hepatol
(N Y). 2015;11(12):847-849.
21. Isabel Garrido, Peixoto A, Santos AL, Morais R, Macedo G.
Anti-Reflux Mucosal Ablation: One More Kid in Town for
the Treatment of Gastroesophageal Reflux Disease. GE Port
J Gastroenterol. 2023;31(5):360-363. Published 2023 Dec 12.
doi:10.1159/000535205
22. Hernández Mondragón, Oscar v. et al. Antireflux ablation
therapy (arat), for reflux disease after POEM procedure. early
clinical experience. gastrointestinal endoscopy, volume 91,
issue 6, ab130
23. Shimamura Y, Inoue H, Tanabe M, et al. Clinical outcomes
of anti-reflux mucosal ablation for gastroesophageal reflux
disease: An international bi-institutional study. J Gastroenterol
Hepatol. 2024;39(1):149-156.
24. He J, Yin Y, Tang W, et al. Objective Outcomes of an Extended
Anti-reflux Mucosectomy in the Treatment of PPI-Dependent
Gastroesophageal Reflux Disease (with Video). J Gastrointest
Surg. 2022;26(8):1566-1574.
25. Rodríguez de Santiago E, Sanchez-Vegazo CT, Peñas B, et
al. Antireflux mucosectomy (ARMS) and antireflux mucosal
ablation (ARMA) for gastroesophageal reflux disease:
a systematic review and meta-analysis. Endosc Int Open.
2021;9(11):E1740-E1751. Published 2021 Nov 12.
26. Sumi K, Inoue H, Kobayashi Y, et al. Endoscopic treatment of
proton pump inhibitor-refractory gastroesophageal reflux disease
with anti-reflux mucosectomy: Experience of 109 cases.
Dig Endosc. 2021;33(3):347-354.
27. Lu J, Chen F, Lv X, et al. Endoscopic construction of an
antireflux mucosal barrier for the treatment of GERD: a pilot
study (with video). Gastrointest Endosc. 2023;98(6):1017-
1022.

Download Tables, Images & References

Dispatches from the GUILD Conference, Series #67

What do Gastroenterologists Need to Know About Stomas?

April 2025 • Volume XLIX, Issue 4
Gilad Alon,Michael Goldenshluger,Stefan D. Holubar,Miguel Regueiro

Read Article

Intestinal stomas, whether from the small or large bowel, are the cornerstone of the surgical management of various gastrointestinal conditions, particularly in patients with inflammatory bowel disease (IBD) and rectal cancer. This review provides an overview of stoma types, indications, complications, and the critical role of preoperative and postoperative care. This highlights the necessity for collaboration between colorectal surgeons and gastroenterologists to optimize surgical planning, manage complex cases, and prevent complications. Stomas play a pivotal role in treating refractory diseases, high-risk surgical scenarios, and emergencies. Comprehensive care involving multidisciplinary teams that include stoma nurses, dietitians, and mental health professionals is essential for addressing stoma-related challenges, minimizing complications, and improving patient outcomes. By integrating medical and surgical expertise, healthcare teams can empower patients to adapt successfully and maintain high quality of life.

Introduction

Intestinal stomas involve the surgical exteriorization of either the small or large bowel through the anterior abdominal wall. These stomas, whether small or large, play vital roles in the treatment and management of various gastrointestinal diseases. In the United States, the estimated number of patients living with a stoma (ostomates) ranges from 750,000 to 1 million, with approximately 150,000 new ostomies constructed each year.1 A comprehensive understanding of the surgical planning and decision-making processes involved in constructing ostomies, the different types of stomas, their potential complications, and the preoperative and postoperative care required, are essential for the successful treatment of patients with ostomies.2

1. Know the anatomyExactly what kind of stoma?
How much proximal and distal bowel?
Plans for restoration of intestinal continuity?
2. Stoma complicationsPoor pouching? Refer to Ostomy nursing
Anatomic issue? Refer to surgeon
Manifestation of systemic disease?
Treat as appropriate
3. High output enterostomyAvoid sugar (diarrheogenic)
Isotonic oral rehydration solutions
Stool bulking “thicken it up”
Antimotility agents “slow it down”
Parental fluid and/or nutritional support
as needed
Table 1. Key points:
What do Gastroenterologists Need to Know About Stomas?

A summary of key points and stoma-related terms is presented in Tables 1 and 2. Stoma is the Greek word for mouth and is defined as an artificial opening of a hollow organ; an ostomy refers to an opening of the bowel brought to the skin to allow egress of intestinal fluids through the os, but “-ostomy” may also refer to tubes placed in GI organs that cannot reach the skin (i.e., duodenostomy, gastrostomy).

Types of Stomas

Large bowel stoma: colostomy

Colostomies are constructed using the large intestine, most commonly the distal transverse, descending, or sigmoid colon. The more distal the colostomy, the better the functional outcomes, as stool consistency becomes more dehydrated, and stool frequency decreases.3 Compared to small bowel ostomies, colostomies have firmer stool consistency, easier pouch management, and a lower incidence of systemic complications such as electrolyte disturbances and dehydration, which are more common in small bowel ostomies.3 Colostomies generally offer better functionality given the ability of the large bowel proximal to the colostomy to absorb water and electrolytes with a resultant neutral pH (as opposed to the mildly acidic succus from ileostomies which results in universal skin irritation and the need for maturation of the os in a budded manner). Given the neutral pH of stool from a colostomy, it may be budded (matured) and protrude a few centimeters above the skin or lie flush with the skin surface, depending on patient-specific factors, such as body habitus, surgical technique, and the bowel’s length of reach to make a tension-free colocutaneous anastomosis whenever possible. Right colonic or proximal transverse colostomies are generally avoided, resulting in feculent diarrheal output as opposed to the thicker stool from distal colostomies or non-feculent succus entericus output from an ileostomy (which is generally preferred compared to a right-sided colostomy). A rare form of large-bowel stoma is an appendicostomy which may be used for antegrade colonic irrigation (i.e., the Malone antegrade continent enema [MACE] procedure).

Colostomies (Figure 1) can be fashioned as a loop colostomy, an end colostomy, or a “double barrel” colostomy depending on the clinical indication and surgical approach. A mucus fistula is an ostomy of the defunctionalized distal segment that is matured as a complete or partial opening to allow drainage of mucus and secretions from the distal segment and is critical to decompress the distal segment when a distal obstruction is present. An end colostomy is typically chosen when making a permanent colostomy, such as during an abdominoperineal resection for low rectal cancer or may be chosen in an emergency surgery after a segmental resection (e.g., surgery for perforated diverticulitis). In contrast, a loop colostomy or double-barrel colostomy may be selected when future bowel reconstruction is anticipated or when there is a need for distal decompression. A double-barrel colostomy is distinguished from a loop colostomy by its separation into two distinct stomas, one for the proximal bowel to divert feces and the other for the distal bowel to allow mucus drainage, whereas a loop colostomy typically involves a single stoma with two openings.

CategoryOrganOstomy
OstomiesJejunumJejunostomy
IleumIleostomy
AppendixAppendicostomy
ColonColostomy
Urinary tractUrostomy
TubesStomachGastrostomy
DuodenumDuodenostomy
Intestinal anastomosesSmall bowelEnteroenterostomy
IleocolicIleocolostomy
ColonColocolostomy
ColorectumColoproctostomy
Total colectomyIleoproctostomy
(aka ileorectal anastomosis)
Table 2. Summary of Ostomy Terminology

Small bowel stoma: enterostomy (Ileostomy and Jejunostomy)

Small bowel ostomies such as ileostomies and jejunostomies are constructed using the small intestine. They are most commonly fashioned from the terminal ileum but can be created from any part of the small bowel, depending on the clinical scenario. Generally, the more proximal the small bowel ostomy, the higher the sensitivity to systemic complications.1 Ileostomies are indicated for conditions requiring bowel diversion or resection of either the small or large intestine when anastomosis to restore bowel continuity is not feasible, either temporarily or permanently. Jejunostomies are made from the more proximal jejunum and avoided as much as possible due to their morbid nature, given their significantly higher output of acidic, electrolyte-rich succus entericus resulting in total parenteral nutrition dependence and may be classified as low- or high- jejunostomies, less than or greater than 30 cm from the ligament of Treitz, respectively. 

Compared to colostomies, ileostomies result in liquid to semi-liquid stool output (ideally yogurt consistency) owing to the lack of colonic reabsorption of water and electrolytes. Consequently, patients with ileostomies are at a higher risk of dehydration and electrolyte disturbances (e.g., hypokalemia and hyponatremia), as well as local issues such as skin irritation due to frequent stool output. Therefore, ileostomies must be matured such that the os is ideally 2 cm above the skin in a “spigot” manner (Figure 2) such that the stool egresses directly into the ostomy appliance bag to minimize skin irritation. Ileostomies (and jejunostomies) may be fashioned as an end ileostomy, loop ileostomy, or end loop. 

An end ileostomy (Figure 2) involves bringing the ileum through the abdominal wall to create a single stoma and is often permanent and is typically performed after total proctocolectomy or when bowel continuity cannot be restored. End ileostomies may be fashioned in several ways (Figure 3). An end-loop ileostomy made by bringing a loop proximal to the stapled-off distal segment is brought out, often chosen when there are difficulties in getting the bowel to reach 2 cm above the surface due to the shorter divided mesentery associated with a true end ileostomy, while in an end-loop the intact mesentery supplying the loop allows for additional length. When there is a distal obstruction, an end ileostomy may be performed with a mucus fistula as an additional small opening to allow drainage of mucus and secretions from the distal bowel segment when necessary. 

A loop ileostomy (Figure 4) is commonly used for temporary bowel diversion to protect the downstream anastomosis after intestinal resection. A loop of the small bowel is brought to the surface and opened, creating a stoma with two openings; the proximal limb diverts stool to the exterior, while the distal limb allows mucus drainage from the downstream bowel. Loop ileostomies are typically easier to reverse than end ileostomies, making them the preferred choice for temporary diversion. 

Continent ileostomy (Figure 5), although less commonly performed today, involves the creation of an internal reservoir, such as a Kock pouch. This reservoir allows stool to be stored and drained via intermittent catheterization. Continent ileostomies are typically chosen by patients who wish to avoid a traditional end ileostomy and are not candidates for restorative surgery with an ileal pouch-anal anastomosis (IPAA) after total proctocolectomy or personal preference. 

Indications for Stoma Creation

Temporary diversion

Temporary bowel diversion is frequently required in specific clinical scenarios in which protecting the distal anastomosis is critical. For example, in patients undergoing low rectal anastomosis after neoadjuvant radiotherapy or after IPAA, a temporary stoma diverts the fecal stream to allow the pouch to heal. Risk factors for anastomotic leakage include high-dose/prolonged corticosteroids, malnutrition, anemia, smoking, and other risk factors.4 Of note, ileostomies do not decrease anastomotic leak rates but rather decrease the severity of leaks when they occur, thus allowing less invasive treatment and facilitating successful leak management and healing by methods such as percutaneous drains and endoluminal vacuum therapy.5-8 In cases of extensive perianal disease, such as severe perianal Crohn’s disease or complex fistulas, temporary diversion may be necessary to facilitate perineal wound healing and reduce ongoing inflammation. Similarly, in the presence of active pelvic infections and inflammation — such as colovesical and colovaginal fistulas secondary to diverticulitis or malignancy — temporary diversion before or at the time of definitive surgical repair is often required to facilitate successful restoration of intestinal continuity.9

Permanent ostomies

In some cases, a permanent ostomy is planned from the outset, whereas in others, an initial temporary ostomy may become permanent due to unforeseen clinical factors or patient preference. Abdominoperineal resection (APR) is a common indication for permanent colostomy in patients with low rectal cancer, where sphincter preservation is not feasible. Another scenario requiring permanent bowel diversion is total proctocolectomy without ileal pouch creation, typically performed in patients with ulcerative colitis or familial adenomatous polyposis who are either not candidates for or decline an ileal pouch-anal anastomosis. 

Emergencies

In emergency settings, primary bowel reconstruction is often contraindicated, which necessitates stoma creation. Emergency bowel resection, frequently required for patients presenting with perforation, obstruction, or ischemia, may necessitate a stoma when factors such as hemodynamic instability, active infection, or poor tissue perfusion preclude a safe anastomosis. Trauma, whether from penetrating or blunt abdominal injuries, may also warrant temporary or permanent stoma creation to manage bowel injuries and prevent further complications.

Stomas in Inflammatory Bowel Disease (IBD)

Despite advances in medical therapy, including biologics and small molecules, a subset of patients with IBD still require surgical intervention. Surgery remains necessary for those with refractory disease, abdominal complications such as strictures, perforations, or abscesses, and severe perianal Crohn’s disease.10-12 It is estimated that approximately 20–30% of ulcerative colitis patients will require a colectomy during their lifetime, while up to 58% of Crohn’s disease patients will undergo at least one major abdominal surgery within 20 years of diagnosis.11-13 

Stomas, typically ileostomies, are often indicated in IBD cases where anastomosis is either high-risk or should be avoided. Factors that increase the risk of anastomotic leakage include severe malnutrition, prolonged steroid use, and emergency surgical indications such as abdominal sepsis or bowel obstruction.

Stoma in Ulcerative Colitis

Total proctocolectomy is typically performed with or without IPAA for ulcerative colitis (UC). To optimize outcomes and reduce morbidity, this procedure is usually staged. The 3-staged approach is most common these days, starting with a total abdominal colectomy with end ileostomy (Stage 1), leaving the rectum intact, followed by a completion proctectomy with IPAA and temporary diverting loop ileostomy (Stage 2); finally, diverting loop ileostomy reversal (Stage 3) after pouch healing is confirmed. Other staging strategies include a 2-stage, starting with a total proctocolectomy with IPAA and temporary loop ileostomy (Stage 1), followed by ileostomy reversal, and a modified 2-stage which is similar to a 3-stage, but the diverting loop ileostomy is omitted in the 2nd stage. Of note, approximately 10% of UC patients after Stage 1 of a 3-stage will have such a dramatic improvement in their health and quality of life they choose to keep it permanently and forgo IPAA, while others who are not candidates for IPAA choose a continent ileostomy. Another 5-10% of patients will require pouch excision and end ileostomy due to treatment-refractory leaks or Crohn’s-like disease of the pouch.

AgentAdult Oral DoseMaximum Daily DoseNotes
Loperamide1 – 4 two mg tablets or caplets (not capsules)  QID 30 min. before meals & QHS16 tabsOTC but can also prescribe for some
Diphenoxylate-atropine1 – 2 2.5 mg tabs  QID 30 min. before meals & QHS 8 tabsOpioid script, non-sedating
Codeine15 – 60 mg  QID 30 min. before meals & QHS240 mgOpioid script
Deodorized tincture of opium0.3 – 0.6 mL sublingual  QID 30 min. before meals & QHS6 mLOpioid script
Octreotide300 – 1200 ug IV/day divided1200 ugProvided in TPN; monitor LFTs
Sandostatin10, 20, or 30 mg IM q28 days30 mg/ monthDepot injection; monitor LFTs & glucose
Table 4. Antimotility Agents

Stoma in Crohn’s disease

In Crohn’s disease, stomas are frequently necessary to manage complications such as strictures, fistulas, abscesses, and perforations.14,15 “Temporary” diversion with an ileostomy or colostomy may also be required in severe perianal disease to facilitate wound healing and symptom control, but become permanent in the vast majority.16,17 Additionally, in high-risk conditions such as malnutrition or sepsis, primary anastomosis carries an unacceptably high failure rate, making stoma creation the preferred surgical option.5 Ultimately, the decision to create a stoma in IBD should be guided by both the patient’s clinical status and long-term disease trajectory.

Endoscopy in Stoma Patients

Prior to performing ileoscopy or colonoscopy in ostomates, it is important for the endoscopist to focus on the exact anatomy of the ostomy and the segments that need endoscopic interrogation. For example, if a patient has undergone Hartmann’s colostomy, it also has a distal segment known as Hartmann’s pouch (rectal stump), which requires assessment prior to colostomy reversal and routine endoscopic surveillance if the stump is kept in place permanently. For ileostomies, it should be kept in mind the bowel wall is thinner and more prone to incidental perforation compared with the colon. When scoping an apparent loop ileostomy, it may be an end-loop, and in this case, excessive pressure trying to intubate the stapled distal limb may result in perforation and enterocutaneous fistula formation.

Stoma Complications

The construction of an ostomy, whether a small bowel or colonic stoma, is associated with a substantial morbidity rate, with reported complication rates ranging from 20% to 80%.1 Among the most common issues are peristomal skin complications and parastomal hernias. One large population-based study analyzing over 4,200 patients found an overall surgical complication rate of 37% in elective ostomy cases and 55% in emergency ostomy cases.18

Peristomal skin irritation, hyperplastic granulation tissue, and mucocutaneous separation

(Figure 6) Peristomal skin is particularly vulnerable to irritation and breakdown due to stool leakage or ill-fitting appliances. Contact dermatitis may occur secondary to appliance adhesive. Hyperplastic granulation tissue may result from the use of a tight-fitting appliance. Treatment involves optimizing pouching techniques, applying barrier creams, and revising the stoma if necessary. Mucocutaneous separation and peristomal ulceration (Figure 7) may be thought of as a failure of enterocutaneous anastomosis to heal, and fastidious skin care may expedite healing.

Stoma retraction and strictures

(Figure 7) Retraction below the skin level can cause a poor fit and difficulty in waste elimination. Less commonly, stenosis  may develop because of mechanical causes (such as scar formation) or inflammatory changes, leading to impaired stoma function. Management options include dietary modification, dilation, or surgical revision.

Peristomal fistulae

(Figure 8) Peristomal infections can develop due to local inflammation or stool leakage, potentially resulting in abscess or fistula formation. Management may require surgical drainage and optimization of stoma care.

Peristomal pyoderma gangrenosum

(Figure 9) Chronic irritation can lead to inflammatory skin conditions including pyoderma gangrenosum (PG), which presents as painful ulcerations around the stoma. Management typically requires topical or intralesional corticosteroids and may require surgical revision in refractory cases. Surgical repositioning of the stoma is performed in severe cases, particularly when bowel continuity cannot be restored but is prone to recurrence if the underlying inflammatory disorder is not addressed with systemic advanced therapies. A stepwise algorithmic approach for management and treatment of peristoma PG is shown in Figure 10. 

Prolapse and parastomal hernias

(Figure 11) Excessive protrusion of the stoma beyond the abdominal wall may lead to cosmetic concerns, difficulty in pouching, ischemia, or even bowel obstruction. Treatment depends on the severity and ranges from non-surgical interventions (e.g., manual reduction, application of sugar to draw out the edema from the prolapsed segment, and support belts) to surgical revision. Prolapse is typically secondary to a parastomal hernia.

A parastomal hernia is defined as an incisional hernia that occurs at the site of an abdominal wall stoma. The reported incidence of parastomal hernias varies widely, depending on factors such as the length of follow-up and the type of stoma created. The incidence of end colostomies is slightly higher, reaching up to 48%, whereas that of loop ileostomies is reported to be up to 30.8%.18,19 Although most parastomal hernias are asymptomatic and can therefore be treated conservatively, parastomal hernias can significantly impair the quality of life and cause symptoms such as pain, discomfort, and, in severe cases, bowel obstruction. Compared with other incisional hernias, parastomal hernias are more challenging to repair because of the permanent defect in the abdominal wall created by the stoma. This complexity often necessitates careful preoperative planning and use of specialized surgical techniques for hernia repair.20,21

Nutrition in Ostomates

Dietary adjustments for ostomates can be divided into the early and late postoperative phases. In the early phase, the primary considerations were the patient’s preoperative nutritional status and underlying condition. In cases of severe metabolic deconditioning, 10–14 days of enteral or parenteral nutritional therapy may be beneficial before surgery and directly affect postoperative recovery.22 Early physiological enteral nutrition after surgery improves intestinal adaptation, preserves the intestinal flora and enteric immune system, and is cost effective when compared with parenteral feeding.22,23 Postoperatively, the diet is usually introduced gradually and typically consists of low-fiber foods to minimize stool production, reduce strain, and prevent obstruction, as surgical manipulation can lead to bowel edema.24 

In the long term, dietary adjustments for ostomates should be individualized based on three key factors: type of stoma, output volume, and the patient’s underlying condition. Generally, the aim is to maintain a healthy and rich diet, including all nutrients and fibers, as long as stoma function is optimal. After the initial recovery period (typically 6-8 weeks), it is recommended that new foods be introduced slowly and in small quantities, one at a time, as it simplifies the process of eliminating them if issues arise.25 

Dietary adjustments for colostomy patients

The diet of patients undergoing colostomy tends to be easier to manage than that of patients undergoing ileostomy. For long-term management, especially for patients with a permanent colostomy, maintaining a healthy BMI is crucial, as obesity and weight gain have been associated with colostomy retraction and symptomatic parastomal hernias.15 Although no specific diet has been proven effective after colostomy formation, a diet rich in complex carbohydrates and low in fat (while incorporating medium-chain triglycerides) may be beneficial. It is important to monitor for potential deficiencies in fat-soluble vitamins (A, D, E, and K), as well as in fatty acids. After the early postoperative period, including higher-fiber foods such as brown rice or whole wheat bread for patients with colostomy may help prevent constipation.26

Dietary adjustments in patients with ileostomies

After the formation of an ileostomy and during the early postoperative period, stoma output is usually unpredictable and may remain elevated for 1–3 months. When the entire colon is absent or not in continuity, patients lose the endogenous vitamins and nutrients typically produced by the gut microbiota, including vitamins K and B, folic acid, and short-chain fatty acids.26 In addition, the absorption of fat and niacin is much lower than that in patients with a colostomy. Hence, these patients should be monitored for their fat intake and the levels of fat-soluble vitamins (A, D, E, and K), along with vitamin B12, which is absorbed in the ileum by intrinsic factors. For ileostomy patients, especially those with a high-output stoma, the energy requirements may increase by up to 30%.27 To meet these needs, it is essential to increase the caloric content of the diet, which can be achieved either through dietary modifications or oral nutritional supplements. During the first year of recovery, patients may require multivitamin supplements.25 To minimize fluid loss and reduce gastric fluid production, it is recommended that patients avoid drinking fluids 30 min before and after meals. The type of fluid consumed is also important, as carbonated beverages can increase the gas in the stoma bag, leading many patients to limit or avoid them. It is helpful to reduce the amount of food consumed per meal, while increasing the number of meals throughout the day.28 

After the first 6–8 weeks post-surgery, patients should be encouraged to introduce more fruits and vegetables, provided their stoma output has normalized in both volume and consistency.24 Tolerance to fiber varies among individuals, with some patients being able to resume a high-fiber diet, while others may need to gradually reintroduce these foods or avoid certain items altogether. For ileostomy patients, some foods should be consumed with caution, as they may pose a risk of causing stoma blockages (popcorn, apple peels, whole corn, bean sprouts, dried fruit, and nuts) and excessive gas or unpleasant odors (beans/pulses, cabbage, broccoli, cauliflower, mushrooms, onions, and alcohol).28 Additionally, patients with ileostomy may develop lactose intolerance after surgery due to changes in gut function. Therefore, they should avoid dairy products if they experience abdominal cramps or watery output.

High output enterostomy (HOE) and electrolyte management

Dehydration and electrolyte imbalances are the leading causes of hospital readmission following ileostomy formation and are responsible for up to 10% of readmissions within 60 days post-surgery; the most common postoperative losses in patients undergoing ileostomy are fluid, sodium, potassium, and magnesium.29,30 Table 3 shows electrolyte replacement options. Of note, magnesium sulfate supplements are diarrheogenic, and Mag Plus Protein (Miller Pharmaceutical Group) may be recommended to avoid obligate fluid losses associated with magnesium sulfate supplementation. During the first 6–8 weeks, patients may lose 1200–2000 ml of fluid and 120–200 mmol of sodium per day. However, after approximately eight weeks, the ileum typically undergoes adaptation, leading to a reduction in fluid losses.28 During the immediate postoperative period; therefore, close monitoring of renal function and electrolyte balance is essential. These assessments should be repeated at follow-up appointments within a month or sooner if any clinical signs arise. A stepwise algorithmic approach for managing HOE is recommended (Figure 12), which focuses on isotonic oral fluid repletion, stool bulking, and antimotility agents. A summary of antimotility agents is shown in Table 4. Patients with HOE, defined as producing >1500 ml/day after adaptation, are recommended to avoid sugary drinks and foods that cause osmotic diarrhea, avoid hypotonic fluids, and instead consume an additional 1000 ml of oral rehydration solution to replace the lost electrolytes.31 Unlike typical physiological responses, patients should be advised against increasing fluid intake of hypotonic fluids such as water, tea, or juice, as these hypotonic fluids may cause greater fluid loss from the stoma and instead use a rehydration solution. 

Role of Multidisciplinary Care

Patients with ostomies, especially IBD, who require an ostomy, should be cared for by a multidisciplinary team that includes a gastroenterologist, colorectal surgeon, dietitian, pharmacist, social worker, psychologist, and a stoma therapist. Early involvement of colorectal surgeons is crucial for discussing the procedure, setting expectations, reassessing nutritional status, and possibly offering nutritional prehabilitation through enteral or parenteral feeding.

Stoma nurses are essential for providing education, support, and managing various stoma-related complications. The involvement of a mental health specialist and an ostomy nurse has been shown to enhance ostomy acceptance, reduce complications, improve quality of life, and are associated with shorter hospital stays.32

Conclusion

Enterostomies remain a cornerstone of the surgical management of gastrointestinal conditions, particularly in patients with complex IBD. The creation of an intestinal stoma can profoundly reshape a patient’s life, often presenting unique challenges and risks, including complications and potential impacts on the quality of life. Enterostomies play a critical role in managing refractory diseases, complications, and surgical recovery in patients with IBD.

The success of stoma creation and its subsequent management relies heavily on the collaborative expertise of a multidisciplinary team that includes colorectal surgeons and gastroenterologists. This partnership ensures tailored surgical planning, precise execution, and vigilant postoperative care, which are essential for minimizing complications and supporting patients in achieving the best possible outcome. By integrating medical and surgical approaches, healthcare teams can empower ostomy patients to adapt and lead fulfilling lives, even in the face of chronic illnesses. 

References

1. Malik T, Lee MJ, Harikrishnan AB. The incidence of stoma related morbidity – a systematic review of randomised controlled trials. Ann R Coll Surg Engl. Sep 2018;100(7):501-508. doi:10.1308/rcsann.2018.0126

2. Davis BR, Valente MA, Goldberg JE, et al. The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for Ostomy Surgery. Dis Colon Rectum. Oct 1 2022;65(10):1173-1190. doi:10.1097/DCR.0000000000002498

3. Gooszen AW, Geelkerken RH, Hermans J, Lagaay MB, Gooszen HG. Quality of life with a temporary stoma: ileostomy vs. colostomy. Dis Colon Rectum. May 2000;43(5):650-5. doi:10.1007/BF02235581

4. Guyton K, Kearney D, Holubar SD. Anastomotic Leak after Ileal Pouch-Anal Anastomosis. Clin Colon Rectal Surg. Nov 2021;34(6):417-425. doi:10.1055/s-0041-1735274

5. Neary PM, Aiello AC, Stocchi L, et al. High-Risk Ileocolic Anastomoses for Crohn’s Disease: When Is Diversion Indicated? J Crohns Colitis. Jul 25 2019;13(7):856-863. doi:10.1093/ecco-jcc/jjz004

6. Alipouriani A, Hull T, Lipman J, et al. Diagnosis and treatment of primary ileal pouch leaks: a 27-year experience at a referral center. J Gastrointest Surg. Jun 2024;28(6):860-866. doi:10.1016/j.gassur.2024.03.015

7. Alipouriani A, Lavryk O, Lipman J, et al. Ileoanal pouch salvage rates with endoluminal vacuum therapy for early vs late anastomotic leaks. J Gastrointest Surg. Dec 2024;28(12):1976-1982. doi:10.1016/j.gassur.2024.09.009

8. Uchino T, Lincango EP, Lavryk O, et al. Long-term ileoanal pouch survival after pouch urinary tract fistulae. Tech Coloproctol. Jun 25 2024;28(1):72. doi:10.1007/s10151-024-02948-w

9. DeLeon MF, Sapci I, Akeel NY, Holubar SD, Stocchi L, Hull TL. Diverticular Colovaginal Fistulas: What Factors Contribute to Successful Surgical Management? Dis Colon Rectum. Sep 2019;62(9):1079-1084. doi:10.1097/DCR.0000000000001445

10. Barnes EL, Lightner AL, Regueiro M. Perioperative and Postoperative Management of Patients With Crohn’s Disease and Ulcerative Colitis. Clin Gastroenterol Hepatol. May 2020;18(6):1356-1366. doi:10.1016/j.cgh.2019.09.040

11. Holubar SD, Pendlimari R, Loftus EV, Jr., et al. Drivers of cost after surgical and medical therapy for chronic ulcerative colitis: a nested case-cohort study in Olmsted County, Minnesota. Dis Colon Rectum. Dec 2012;55(12):1258-65. doi:10.1097/DCR.0b013e31826e4f49

12. Patel KV, Darakhshan AA, Griffin N, Williams AB, Sanderson JD, Irving PM. Patient optimization for surgery relating to Crohn’s disease. Nat Rev Gastroenterol Hepatol. Dec 2016;13(12):707-719. doi:10.1038/nrgastro.2016.158

13. Holubar SD, Lightner AL, Poylin V, et al. The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Surgical Management of Ulcerative Colitis. Dis Colon Rectum. Jul 1 2021;64(7):783-804. doi:10.1097/DCR.0000000000002037

14. Duraes LC, Holubar SD, Lipman JM, et al. Redo Continent Ileostomy in Patients With IBD: Valuable Lessons Learned Over 25 Years. Dis Colon Rectum. Mar 1 2023;66(3):419-424. doi:10.1097/DCR.0000000000002619

15. McKenna NP, Bews KA, Habermann EB, Dozois EJ, Lightner AL, Mathis KL. What Factors Are Associated With the Eventual Need for an Ileostomy After Total Abdominal Colectomy and Ileosigmoid or Ileorectal Anastomosis for Crohn’s Colitis in the Biologic Era? Dis Colon Rectum. Apr 2020;63(4):504-513. doi:10.1097/DCR.0000000000001556

16. Lightner AL, Steele SR, Delaney CP, et al. Colonic disease recurrence following proctectomy with end colostomy for anorectal Crohn’s disease. Colorectal Dis. Sep 2021;23(9):2425-2435. doi:10.1111/codi.15777

17. Holubar SD, Keller J, Cooper L. When Patients With IBD Require an Ostomy: Evidence-Based Answers to 10 Common Clinical Questions in IBD Surgery. Am J Gastroenterol. Feb 1 2025;120(2):268-271. doi:10.14309/ajg.0000000000002914

18. Shabbir J, Britton DC. Stoma complications: a literature overview. Colorectal Dis. Oct 2010;12(10):958-64. doi:10.1111/j.1463-1318.2009.02006.x

19. Obi M, Beffa L, Melland-Smith M, et al. The rate of ileostomy site incisional hernias: more common than we think? Hernia. Dec 2024;28(6):2311-2320. doi:10.1007/s10029-024-03163-0

20. Hansson BM, Slater NJ, van der Velden AS, et al. Surgical techniques for parastomal hernia repair: a systematic review of the literature. Ann Surg. Apr 2012;255(4):685-95. doi:10.1097/SLA.0b013e31824b44b1

21. Israelsson LA. Parastomal hernias. Surg Clin North Am. Feb 2008;88(1):113-25, ix. doi:10.1016/j.suc.2007.10.003

22. Fernandez-Galvez A, Rivera S, Duran Ventura MDC, de la Osa RMR. Nutritional and Educational Intervention to Recover a Healthy Eating Pattern Reducing Clinical Ileostomy-Related Complications. Nutrients. Aug 20 2022;14(16)doi:10.3390/nu14163431

23. Mukhopadhyay A, Maity D, Dey R, Choudhury KB, Das G, Bhattacharya U. Can Postoperative Nutrition be Favourably Maintained by Oral Diet in Patients with Emergency Temporary Ileostomy? A Tertiary Hospital Based Study. J Clin Diagn Res. Dec 2015;9(12):PC04-8. doi:10.7860/JCDR/2015/15220.6879

24. Migdanis A, Migdanis I, Koukoulis GD. Nutritional Considerations in Colorectal Surgery in Diverting Ileostomy Patients: A Review. Cureus. Nov 2023;15(11):e48102. doi:10.7759/cureus.48102

25. Michonska I, Polak-Szczybylo E, Sokal A, Jarmakiewicz-Czaja S, Stepien AE, Deren K. Nutritional Issues Faced by Patients with Intestinal Stoma: A Narrative Review. J Clin Med. Jan 8 2023;12(2)doi:10.3390/jcm12020510

26. Fulham J. Providing dietary advice for the individual with a stoma. Br J Nurs. Jan 24-Feb 13 2008;17(2):S22-7. doi:10.12968/bjon.2008.17.Sup1.28146

27. Medlin S. Nutritional and fluid requirements: high-output stomas. Br J Nurs. Mar 22-Apr 11 2012;21(6):S22-5. doi:10.12968/bjon.2012.21.Sup6.S22

28. Gasche R. Diet and stoma care. Br J Community Nurs. Sep 2 2022;27(9):444-448. doi:10.12968/bjcn.2022.27.9.444

29. Akesson O, Syk I, Lindmark G, Buchwald P. Morbidity related to defunctioning loop ileostomy in low anterior resection. Int J Colorectal Dis. Dec 2012;27(12):1619-23. doi:10.1007/s00384-012-1490-y

30. Liu C, Bhat S, Sharma P, Yuan L, O’Grady G, Bissett I. Risk factors for readmission with dehydration after ileostomy formation: A systematic review and meta-analysis. Colorectal Dis. May 2021;23(5):1071-1082. doi:10.1111/codi.15566

31. Cuerda C, Pironi L, Arends J, et al. ESPEN practical guideline: Clinical nutrition in chronic intestinal failure. Clin Nutr. Sep 2021;40(9):5196-5220. doi:10.1016/j.clnu.2021.07.002

32. Levy LC, Coburn ES, Choi S, Holubar SD. The management of the hospitalized ulcerative colitis patient: the medical-surgical conundrum. Curr Opin Gastroenterol. Jul 2020;36(4):265-276. doi:10.1097/MOG.0000000000000637

Download Tables, Images & References

Nutrition Reviews in Gastroenterology, SERIES #22

Nutrition Therapies for Managing Gastrointestinal Symptoms During Pregnancy 

April 2025 • Volume XLIX, Issue 4
Christine L. Scarcello,Kelly Issokson,Puja V. Khanna

Read Article

Gastrointestinal symptoms of pregnancy are common and can interfere with quality of life and the ability to consume adequate oral intake. The occurrence of symptoms varies throughout pregnancy; while nausea and vomiting predominantly affect patients during the first trimester, other symptoms may progressively worsen throughout the length of gestation without relief until the postnatal period. Common symptoms prevalent during pregnancy include nausea and vomiting, gastroesophageal reflux, constipation, and diarrhea. Clinicians can introduce nutritional interventions for the management of mild symptoms prior to pharmacologic intervention, but it is important to monitor for adequate relief. Individuals with chronic GI disorders – such as inflammatory bowel disease, gastroparesis, metabolic dysfunction-associated steatotic liver disease, and irritable bowel syndrome – face an increased risk for malnutrition and may require ongoing care from a gastroenterologist and a registered dietitian during pregnancy. 

Introduction 

The forty-week period of gestation is a time of heightened need for nutritional optimization for both the parent and developing fetus. Changes in the gastrointestinal (GI) tract result from hormonal and physiologic intra-abdominal adaptations during pregnancy and may quickly affect quality of life as well as adequate oral nutrition. The American College of Obstetrics and Gynecology (ACOG) and former Institute of Medicine (IOM) recommendations for specific gestational weight gain ranges for pregnancy are based on pre-pregnancy Body Mass Index (BMI) (See Table 1).1 While these ranges continue to be researched and updated, clinicians should still measure adequacy of weight gain throughout gestation to avoid over- or undernutrition. A recent systematic review of over one million pregnant individuals revealed that 23% did not meet weight gain parameters and 47% exceeded them.2 Monitoring gestational weight milestones is important to prevent poor fetal development and pregnancy outcomes, such as small-for-gestational-age (SGA) infants and preterm birth when undernutrition is present.2 Pregnancy-related GI symptoms can also affect quality of life,and managing mild pregnancy GI symptoms safely and adequately through diet is the recognized first-line treatment (See Table 2).3-6 The purpose of this review is to identify the most common GI symptoms experienced during pregnancy, highlight the first-line nutrition therapies for these ailments, and discuss updates and considerations for pregnant individuals diagnosed with GI disorders. 

BMIClassificationGestational Weight
Gain Goals
<18.5Underweight28-40 lbs
18.5-24.9Normal 25-35 lbs
25-29.9Overweight15-25 lbs
>30Obese11-20 lbs
Table 1.
Gestational Weight Gain per ACOG/IOM Recommendations (2013)1

Common Gastrointestinal
Symptoms During Pregnancy

Nausea and Vomiting

Nausea and vomiting (NV) in pregnancy is the most common GI symptom that affects between 50-90% of pregnant individuals and interferes the most with adequate oral intake and ability to reach pregnancy weight goals.3,4,7 Beginning early in the first trimester and subsiding after 20 weeks, the etiology of NV can be attributed to various hormonal changes.8,9 For example, increased estrogen and human chorionic gonadotropin affect GI motility while progesterone inhibits motility and can cause delayed gastric emptying.8,9 Clinicians should be sure to rule out any other causes of nausea during pregnancy, such as gastroenteritis, biliary disease, gastroparesis (GP), gastroesophageal reflux disease (GERD), peptic ulcers, pancreatitis, hepatitis, pyelonephritis, appendicitis, and irritable bowel syndrome (IBS).4,9 

Common GI SymptomsPractical Nutrition-Related Interventions for Patients
Nausea and Vomiting Texture modification for fruits, vegetables, and proteins to soft and small particle size: fork-tender consistency, blended, steamed, stewed, slow-baked, roasted.  Smaller meals with more frequency to ensure adequate nutrient intake. Supplementation with ginger and Vitamin B6.8 Limit offending foods (based on smell, taste, or texture) that worsen nausea. The use of prenatal vitamin and mineral supplementation one month prior to conception can reduce occurrence and severity.4  
Hyperemesis GravidarumEmphasis on calories and protein at each meal.4   Electrolyte and micronutrient monitoring and replacement.  EN or PN support if intake remains inadequate.
Gastroesophageal Reflux Disorder Smaller meals with more frequency to ensure adequate nutrient intake.  Final meal or snack consumed 2-3 hours before bed. Limit offending foods that worsen symptoms. Common GERD triggers include caffeine/coffee, spicy foods, greasy or high-fat foods, chocolate, peppermint, acidic fruits, heavy creams or gravies, and vinegar. Limit high-volume intake and over-eating. Separating fluids from meals may help reduce the volume of items entering the stomach at one time.
ConstipationIncreased fiber intake if inadequate. Aim for 25-35 grams per day and increase slowly by a few grams each day.  Increased hydration if inadequate. Aim for 60-64 ounces per day.
DiarrheaIncreased soluble fiber intake (e.g., oatmeal, banana, potato). Use of oral rehydration solutions (ORS) if diarrhea is severe/persistent. Review all medications and supplements as some may cause or worsen diarrhea (such as certain antibiotics, laxatives, motility agents, magnesium citrate or oxide).
Table 2. Nutrition-Related Applications for Common GI Symptom Management 

• Nutritional remedies that can be implemented for NV during pregnancy include: 4,7,8,9
• Identifying triggering foods (based on smell, taste, or texture)
• Eating smaller and more frequent meals
• Modifying textures of foods to a smaller particle size
• Choosing bland foods and snacks that are generally higher in protein and lower in fat
• Supplementing with ginger (250 mg capsules four times per day) or vitamin B6 (10-25 mg every eight
hours) before advancing to pharmacologic treatments

If nutrition interventions to reduce NV are unsuccessful, next-line treatment includes H1-receptor antiemetics such as doxylamine, promethazine, and dimenhydrinate.8 Additional pharmacological intervention should be used on a case-by-case basis after identifying the certain risks and benefits of medication use in this population. The use of prenatal vitamin and mineral supplementation at least one month before conception may reduce the occurrence and severity of NV in pregnancy.4 Clinicians should encourage patients to do so, especially in the preconception visit and fertility clinic setting. 

Hyperemesis Gravidarum

Intractable and sustained vomiting – hyperemesis gravidarum (HG) – can lead to severe complications such as metabolic disturbances, dehydration, micronutrient deficiencies, Wernicke’s encephalopathy, and even death from thromboembolism or cardiac arrest.4,10 HG affects a much smaller percentage of pregnancies with various estimates placing its prevalence at approximately 1- 3%.4,7 Research by Fezjo et al. in recent years has shown a causative genetic etiological component of worsening NV and HG related to a hypersensitivity to increased levels of growth and differentiation factor 15 (GDF15) from which future therapies may one day be derived.10,11 Other contributing factors that have shown to be related to HG onset include changes to the amount of progesterone, estrogen, thyroid hormones, and leptin during pregnancy.4 Physiological changes during pregnancy include abnormalities with gastric transit and lower esophageal sphincter (LES) resting pressure, which may increase the severity of NV and risk of developing HG.4  

Manifestations that may present in a clinical exam and that are used to diagnose HG include weight loss (5% or greater), dehydration, ketonuria, orthostasis, micronutrient deficiencies, inadequate oral intake (usually consuming less than 50% of needs), and electrolyte imbalances.4,7 Some severe cases require hospitalization and parenteral administration of fluids and electrolytes. In the acute inpatient setting, a regular diet should be the primary goal with modifications as needed, with the supplementation of enteral nutrition (EN) reserved for those who continue to experience weight loss and are refractory to medical interventions.4 

Malnutrition and inadequate gestational weight gain are concerning consequences of HG.4 It is important to consult a registered dietitian (RD) to monitor for these clinical repercussions and assess when escalation to EN is important. Nasogastric tubes with use of antiemetic medication are preferred first, as post-pyloric feeding tube placement requires imaging for placement confirmation that will expose the fetus to radiation.4 Dietitians should start with polymeric enteral formulas and evaluate tolerance before considering a transition to a semi-elemental enteral formula or an alternative access method. If vomiting remains intractable and there is persistent intolerance to oral and EN support, parenteral nutrition (PN) may become necessary to provide the adequate caloric and protein needs for fetal development and prevention of malnutrition. In lieu of clinical guidelines for this population subset, the decision to escalate to PN must be managed on a case-by-case basis.4 Providing treatment early for NV in pregnancy may help delay the progression to HG, and it is important for clinicians to recognize when escalation of care is essential before severe metabolic disturbances arise.7,8

Gastroesophageal Reflux  

Instances of heartburn, regurgitation, and epigastric pain during pregnancy are often related to GERD, though it is important to rule out other GI disorders that may present with similar symptomatology.9 GERD is a common GI disorder that currently affects 1 in 3 U.S. adults and during pregnancy it has an even higher prevalence of 50-85%with symptoms usually persisting until delivery.8,9,12 Clinical manifestations are diagnosed just as with nonpregnant individuals, with an important note that barium imaging studies should be avoided in pregnant patients due to fetal radiation exposure.9 

The etiology of GERD in pregnancy may be attributed to hormonal changes (for example, progesterone can affect the LES) or physiological changes to intra-abdominal pressure and motility due to an enlarging uterus.8,9,13 The first-line treatment for reflux and associated symptoms includes changes to diet, meal planning, and sleep position.9 Recommendations include:9

• Ceasing intake a few hours before bed
• Eating smaller meals with increased frequency
• Identifying triggering and offending foods and avoiding them
• Raising head of bed during sleep
• Lying on the left side

Schuitenmaker et al. investigated sleep positions on non-pregnant individuals while measuring esophageal pH in 57 adult participants and determined that sleeping in the left lateral decubitus position offered a shorter esophageal acid exposure time and increased acid clearance when compared to right lateral or supine sleep positioning.14 The clinical practice update from the American Gastroenterological Association (AGA) lists modifications to lifestyle and diet as best practice advice.15  Weight loss is the traditional recommendation to reduce GERD symptoms but would not be appropriate to recommend during pregnancy.15 

If the first-line treatment of altered diet and lifestyle change does not improve symptoms, physicians may consider antacids as a second-line therapy.14 Antacids containing aluminum, calcium, and magnesium are considered an acceptable treatment in normal doses, but those containing sodium bicarbonate or magnesium trisilicate are not.16,17 Additional pharmacologic therapy is needed if prior interventions are not effective at managing symptoms on a case-by-case basis. There is a paucity of human study data for GI medications during pregnancy, but some medications have been classified by the Food and Drug Administration (FDA) to be acceptable or lower risk.9,16 The FDA currently does not have a classification for antacids during pregnancy. While antacid use may be beneficial at treating GERD symptoms for 30-50% of pregnant patients, for the rest it may not be sufficient.17 After approaching symptom management with lifestyle change and antacids, clinicians can use histamine-2 receptor blockers, which are classified by the FDA as Category B and have been shown in studies to be safe during pregnancy.17 If unsuccessful, the next approach involves proton pump inhibitors; while classified as Category C, studies have largely indicated their safety during pregnancy even though there is a lack of research around their efficacy at treating symptoms in pregnant patients.17 

Constipation  

Constipation during pregnancy is one of the more common GI symptoms with a global prevalence of 32.4% per recent meta-analysis data.18  Contributing factors in the complex etiology may include decreasing motility and smooth muscle contractility from progesterone production, increased intra-abdominal pressure from an expanding uterus, decreased physical activity level, iron supplementation, and changes to diet such as including more fat- and protein-rich foods to meet nutritional needs during pregnancy.18,19 

Treatment for constipation during pregnancy differs based on the severity of symptoms; mild cases may be improved with lifestyle modifications involving increased dietary fiber intake and adequate hydration.9,18 Clinicians can discuss safe bulking agents such as psyllium fiber or methylcellulose.8 Additionally, education and counseling on how to consume fiber in the diet can be achieved with a referral to an RD. After addressing nutrition and lifestyle changes, further medical management to include osmotic laxatives or stimulants should be started only under the discretion of a physician and for more severe cases.8,18,19 For those suffering with co-occurring GI ailments during pregnancy, osmotic laxatives can worsen bloating, cramps, flatulence, and nausea and therefore may not be a welcomed method of constipation treatment.19  

Hemorrhoids are a common complication of constipation and are prevalent in up to 80% or more of pregnancies.5,8 The etiology can be attributed to the third trimester compression of the rectum from the expanding uterus, prolonged straining during constipation, and inadequate fiber intake to regulate bowel movements.5,8,19The first-line treatment for hemorrhoid prevention include:5

• Increased fiber
• Increased fluid intake
• Improved toileting regimen to limit the amount of time and straining during defecation

Poskus et al. conducted a clinical trial researching the inclusion of dietary strategies for prevention of hemorrhoids in 260 randomized pregnant patients across three medical centers.20The intervention group received education on drinking adequate fluid, increased fiber intake from bran, fruits, vegetables, and nuts, exercising 3-5 times per week for at least 30-60 minutes, spending less than three minutes on the toilet, not ignoring any urgency to use the bathroom, attempting a bowel movement 30-40 minutes after eating, and washing after bowel movements.20 This group showed a significantly reduced occurrence of hemorrhoids by about 50% after receiving the education.20 

Diarrhea

Diarrhea and fecal incontinence are much less common GI symptoms that can occur during pregnancy compared to nausea, vomiting, reflux, and constipation.21 Acute infection is the most common cause for diarrhea during pregnancy so it is important to rule out viral, bacterial, or parasitic infectious etiologies first.21 If acute infection is not present, the noninfectious causes or factors leading to diarrhea during pregnancy may include hormonal changes, changes to diet, increased intra-abdominal pressure, and side effects of prenatal vitamins.21 Clinicians should also consider preexisting conditions such as pelvic floor dysfunction, inflammatory bowel disease (IBD), IBS, lactose intolerance, overflow diarrhea from constipation, a history of anorectal surgeries, or ileal pouch anal anastomosis (IPAA).21  Pregnant individuals with fecal incontinence may benefit from certain lifestyle modifications, which can include pelvic floor muscle training (PFMT) with or without biofeedback therapy.21 A referral to a specialized physical therapist for a PFMT assessment may be useful.21

 The first-line intervention for diarrhea includes a slow introduction and increase in dietary intake of soluble fiber (e.g., banana, oatmeal, potato) or use of psyllium fiber supplementation.21 Important nutrition interventions include consuming smaller and more frequent meals and adequate hydration with electrolytes via oral rehydration solutions (ORS) if diarrhea is frequent and signs and symptoms of dehydration are detected. Intravenous electrolytes and hydration may be necessary for prolonged diarrhea if metabolic abnormalities are present. Excluding whole food groups or overly restrictive diets are not indicated during pregnancy as this may lead to inadequate gestational weight gain or nutritional deficiencies. A consultation with an RD can help ensure patients are consuming adequate nutrition by finding alternatives for any nutrients that are being excluded. 

Pharmacologic intervention for diarrhea during pregnancy should only be used in the most persistent and severe cases, and loperamide is the antidiarrheal most preferred.9,21 It is important to know that diphenoxylate with atropine and bismuth preparations (Pepto-Bismol® and Kaopectate®) are contraindicated during pregnancy due to adverse fetal effects and that probiotics and empiric antibiotics are not routinely used in this population.9,21 

Special Considerations
for Gastrointestinal Disorders

Pregnant individuals with chronic GI disorders may benefit from intervention by their healthcare team during preconception or early pregnancy. The nutrition interventions discussed above for nausea, vomiting, reflux, constipation, and diarrhea would be appropriate for those who have these symptoms superimposed upon their chronic disease, but it warrants a discussion with their healthcare provider and case-by-case evaluation. Below are special considerations during pregnancy for chronic GI disorders (See Table 3).

GI Disorder  Considerations During Pregnancy 
Inflammatory Bowel DiseasePregnancy in active IBD can include increased risks of miscarriage, premature delivery, inadequate gestational weight gain, complications during labor and delivery, and SGA infants.22,23  The AGA recommends remission for 3-6 months prior to conception to reduce flare risk during pregnancy.22  PEN and EEN are safe nutritional interventions during pregnancy. 29,30 Working with an IBD-focused RD can help manage adequate intake and weight gain goals. 
GastroparesisPreconception planning is prudent as GP during pregnancy can lead to nutritional consequences and deficiencies for the patient and fetus.31  Small particle size, low-fat, and low insoluble fiber diets.32  RD consultation to recommend more easily tolerated foods, supplements, and oral nutrition shakes to ensure adequate nutrition. 
Metabolic Dysfunction-Associated Steatotic Liver DiseasePregnancy outcomes with MASLD include higher rates of GDM, gestational hypertension, hypertensive complications, Caesarean sections, preterm births, and postpartum hemorrhage compared to other chronic liver diseases or no liver disease.33  Weight loss is not recommended during pregnancy, but patients can adhere to ACOG/IOM gestational weight gain goals.  Reduction of sugar-sweetened beverages, added sugars, and ultra-processed foods.34
Irritable Bowel Syndrome IBS is a common DGBI that may worsen during pregnancy, theoretically, due to increased hormone production or stress.36  An RD during preconception is beneficial to assess diet quality and liberalization prior to becoming pregnant if currently on a restricted diet. Initiating restrictive diets, such as the high-FODMAP elimination phase if appropriate, should be done under the close guidance of an RD and if no response, then discontinued.36
Table 3. Considerations for Gastrointestinal Disorders During Pregnancy 

Inflammatory Bowel Disease

Risks associated with pregnancy in active IBD include miscarriage, increased risk of premature delivery, inadequate gestational weight gain, complications during labor/delivery, and SGA infants.22,23 Adequacy of nutrition can play a vital role in reducing complications from inadequate gestational weight gain or decreased intake that may occur with active disease, GI complications, or surgical changes in GI anatomy from IBD.22 In one recent cohort study, the risk of inadequate gestational weight gain was higher among those with Crohn’s disease (34.3%) and ulcerative colitis (26.7%) compared to those without IBD (19.4%).24 Twenty percent of participants with IBD in a second cohort study experienced inadequate weight gain and had increased risk for preterm birth, intrauterine growth restriction (IUGR) and SGA.25Poor nutrition in early pregnancy can further affect fetal development from insufficient vitamin and mineral intake, and those with active IBD flaring are at a higher risk of food intolerance and inadequate intake. 

Guidelines from the 2019 AGA IBD Parenthood Project Workgroup recommend women with IBD to be in remission for 3-6 months prior to conception to reduce the risk of flare during pregnancy.22 IBD-trained RDs can help patients navigate dietary concerns, ensure quality nutrition and micronutrient intake, and monitor for appropriate gestational weight gain if flares occur during pregnancy. Many organizations’ recent clinical guidelines and practice updates have recognized the importance of having specialized RDs as part of an IBD interdisciplinary team.26-28 A thorough nutrition assessment can determine whether certain interventions, such as steroid-sparing exclusive enteral nutrition (EEN) or other nutrition therapies, would be beneficial and safe during pregnancy. A recent case report of a 35-year-old woman eight weeks pregnant with moderately severe ileal Crohn’s disease showed clinical remission and weight gain after 6 weeks of the Crohn’s Disease Exclusion Diet (CDED) and partial enteral nutrition (PEN).29 The patient gained appropriate gestational weight (10.3 kg), delivered at 40 weeks, and sustained remission up to 12 weeks postpartum.29 A retrospective observational study of fifteen women with active CD showed that peptide-based EEN was effective at inducing remission in 85.7% of participants without any changes in pregnancy outcomes compared to a non-EEN group.30 The women in the study were pregnant or preparing for pregnancy and had experienced a relapse or complication for which they were refractory to or contraindicated for other treatment modalities.30 In addition to PEN or EEN, specialized therapeutic diets for IBD may also be beneficial for patients as long as they are robust enough to provide adequate micronutrients; monitoring and evaluation by an RD can determine on a case-by-case basis whether a specialized diet is too restrictive for a pregnant individual based on their recall of usual intake. A list of IBD-specific nutrition resources in Table 4 may be beneficial for helping patients expand their diets healthfully during pregnancy.

IBD-Specific ResourcesOrganization
Gut-Friendly RecipesCrohn’s & Colitis Foundation:
gutfriendlyrecipes.org
2020 Consensus Guidelines
for Nutrition		International Organization for the Study of Inflammatory Bowel Disease:
ioibd.org
MyIBDLife Parenthood ProjectAmerican Gastroenterological Association:
myibdlife.gastro.org
Evidence-Based Nutrition TherapiesNutrition Therapy for Inflammatory Bowel Disease:
nutritionaltherapyforIBD.org
Table 4. Resources for Inflammatory Bowel Disease 

Gastroparesis

GP is a chronic disorder of delayed gastric emptying that presents nutritional consequences for the patient and fetus during pregnancy. It is prudent to conduct preconception multidisciplinary planning – including diet education – for those with pre-existing disease who wish to become pregnant.31 There is a lack of data on the efficacy and safety of medications used to treat GP in the pregnant population.31 The 2022 guidelines on gastroparesis from the American College of Gastroenterology (ACG) provide nutrition interventions that include small particle size, low-fat, and low insoluble fiber diets.32 These are appropriate interventions during pregnancy so long as they are not overly restrictive and remain varied enough to provide adequate nutrition for appropriate gestational weight gain. 

Nausea, vomiting, and pain associated with GP may often lead to decreased intake.31 A referral to an RD can help to manage suboptimal intake, oral food intolerances, micronutrient deficiency that may result, and recommendations for whether nutrition support therapies are needed. An RD can provide education on the importance of smaller meals in higher frequency, texture modification for better tolerance, and the use of oral nutrition supplements; an RD can evaluate a patient’s diet pattern and quality to ensure adequacy and recommend the best-absorbed supplements (such as liquids or chewable tablets) that will be better tolerated. 

Metabolic Dysfunction-Associated
Steatotic Liver Disease 

Patients with metabolic dysfunction-associated steatotic liver disease (MASLD or MASH) would benefit from preconception interdisciplinary intervention for management of this chronic disease. Over the last decade, there has been an increase in the incidence of fatty liver diseases among the U.S. population under 40 years old.33 One study looking at 18 million U.S. pregnancies between 2012-2016 identified over 5600 pregnancies with MASLD (previously known as NAFLD) and found significantly more cases of gestational diabetes mellitus (GDM), gestational hypertension, hypertensive complications, Caesarean sections, preterm births, and postpartum hemorrhage compared to other chronic liver diseases or no liver diseases.33 

Weight loss is not recommended during pregnancy but adherence to the ACOG/IOM gestational weight gain is an appropriate intervention. Nutritional interventions include the reduction of sugar-sweetened beverages, added sugars, and ultra-processed foods as these are associated with worsened MASLD status.34 The addition of a Mediterranean-style dietary pattern (which is high in dietary fiber and monounsaturated fatty acids), and reduction of red meat have also been related to a reduced incidence of MASLD.34

Irritable Bowel Syndrome 

IBS is classified as a disorder of gut-brain interaction (DGBI) and characterized by recurrent abdominal pain and altered bowel habits.35 The subgroups of this DGBI are based on bowel status and include IBS with constipation (IBS-C), IBS with diarrhea (IBS-D), and IBS with mixed or alternative bowel habits (IBS-M).35 While there is a lack of extensive study on the effect of pregnancy on IBS, a theoretical association to explain how IBS symptoms may worsen during pregnancy is the change in hormones.36 Increased estrogen during pregnancy can affect gut-brain axis regulatory mechanisms, visceral hypersensitivities, and gut motility.36 Luteal hormone production, which is highest in the first trimester, can affect the migrating motor complex and increase risk of both constipation and small intestinal bacterial overgrowth.36 Increased stress could also play a role in IBS status during pregnancy.36 Regarding pregnancy outcomes, having IBS during pregnancy was associated with increased risks of miscarriage and ectopic pregnancy compared to individuals without IBS, although this information is based on a retrospective trial and more studies of this population are needed.36

A majority of patients with IBS report that their symptoms are food-related, and dietary modification for the exclusion of offending foods (such as gas-producing foods, high lactose content, or foods high in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols known as FODMAPs) remains as first-line treatment for the general IBS population.36,37 In a survey of over 1500 gastroenterologists in the U.S., 60% reported that their patients associate their symptoms with food and were inclined to restrict foods on their own, using dietary modifications that included reducing lactose (33%), eliminating gluten (24%), lowering fat content (6%), or trying low FODMAP diet (2%).37 Half of patients used ‘trial and error’ to determine which foods were problematic.37 Over half of the gastroenterologists reported that they use dietary modification as a first-line treatment strategy to 75% of their patients.37 The most common dietary therapy recommended to patients was a low FODMAP diet (77% of respondents), with high-fiber and lactose-reduced as the next most common (both at 45%).37

The dietary modifications and recommendations for the general IBS population should involve careful consideration during pregnancy to ensure adequacy of nutrient intake.36 Prior to conception, patients with IBS would benefit from consulting with an RD to evaluate baseline adequacy of their diet and to trial diet liberalization. Ongoing follow-ups during pregnancy is recommended if worsening IBS symptoms develop or affect oral intake. Restrictive diets, such as the high-FODMAP elimination phase, should only be started under the close supervision of a registered dietitian.36 If no improvement is observed, the diet should be discontinued. Patients who are on restricted diets for IBS management and become pregnant should also be closely observed for appropriate gestational weight gain and micronutrient adequacy.36 

Conclusion

Clinicians can implement nutritional interventions as useful first-line therapies during pregnancy for many common GI symptoms. Involving an RD during early pregnancy can help those who are experiencing weight loss and inadequate intake from common ailments like nausea, vomiting, reflux, diarrhea, and constipation. Nutrition education during the preconception stages is a beneficial option for those with chronic GI disorders such as IBD, GP, MASLD, and IBS. Patients who are not meeting their gestational weight gain milestones will benefit from frequent RD follow-ups throughout gestation, particularly during the second and third trimesters. There remain gaps in knowledge with a myriad of research opportunities within the pregnant population, especially regarding disease etiology, pharmacologic management, and the role of nutrition in GI disease management. 

References

1. American College of Obstetricians and Gynecologists.
ACOG Committee opinion no. 548: weight gain during
pregnancy. Obstet Gynecol. 2013 Jan;121(1):210-
212.
2. Goldstein RF, Abell SK, Ranasinha S, et al. Association
of Gestational Weight Gain with Maternal and Infant
Outcomes: A Systematic Review and Meta-analysis.
JAMA. 2017;317(21):2207-2225.
3. Grenier LN, Atkinson SA, Mottola MF, Wahoush O,
Thabane L, Xie F, Vickers-Manzin J, Moore C, Hutton
EK, Murray-Davis B. Be Healthy in Pregnancy:
Exploring factors that impact pregnant women’s nutrition
and exercise behaviours. Matern Child Nutr. 2021,
Jan; 17(1) e13068.
4. Austin K, Wilson K, Saha S. Hyperemesis Gravidarum.
Nutr Clin Pract. 2019, Apr; 34(2): 226-241.
5. Rao S, Qureshi WA, Yan Y, Johnson D. Constipation,
Hemorrhoids, and Anorectal Disorders in Pregnancy.
Am J Gastroenterol. 2022, Oct; 117(10S): p 16-25.
6. Johnson P, Mount K, Graziano S. Functional bowel
disorders in pregnancy: effect on quality of life, evaluation
and management. Acta Obstet Gynecol Scand.
2014, Sept; 93(9): 874-879.
7. Jarvis S, Nelson-Piercy C. Management of nausea and
vomiting in pregnancy. BMJ. 2011, June; 342: d3606.
8. Kothari S, Afshar Y, Friedman LS, Ahn J. AGA
Clinical Practice Update on Pregnancy-Related
Gastrointestinal and Liver Disease: Expert Review.
Gastroenterology. Published online August 12, 2024.
9. Body C and Christie JA. Gastrointestinal Diseases in
Pregnancy. Gastroenterol Clin North Am. 2016, Jun;
45(2):267-283. Copyright © 2016 Elsevier Inc
10. Fezjo MS. Hyperemesis gravidarum theories dispelled
by recent research: a paradigm change for better care
and outcomes. Trends Mol Med. 2024, June; 30(6):
530-540.
11. Fejzo MS, Rocha N, Cimino I. et al. GDF15 linked
to maternal risk of nausea and vomiting during pregnancy.
Nature. 2024, Jan; 625:760–767.
12. Delshad SD, et al. Prevalence of Gastroesophageal
Reflux Disease and Proton Pump Inhibitor-Refractory
Symptoms. Gastroenterology. 2019 Dec; 158(5):
1250-1261.
13. Altuwaijri M. Evidence-based treatment recommendations
for gastroesophageal reflux disease during pregnancy:
a review. Medicine (Baltimore). 2022, Sept;
101(35): e30487.
14. Schuitemaker JM, van Dijk M, Oude Nijhuis
RAB, Smout André JPM, Bredenoord AJ.
Associations Between Sleep Position and Nocturnal
Gastroesophageal Reflux: A Study Using Concurrent
Monitoring of Sleep Position and Esophageal pH and
Impedance. Am J Gastroenterol. 2022, Feb; 117(2):
346-351.
15. Yadlapati R, Chang K, et al. AGA Clinical Practice
Update on the Personalized Approach to the
Evaluation and Management of GERD: Expert Review
Clin Gastroenterol Hepatol. 2022, May; 20(5): 984 –
994
16. Mahadevan U. Gastrointestinal medications in pregnancy.
Best Pract Res Clin Gastroenterol. 2007, Oct;
21(5): 849-877.
17. Altuwaijri, M. Evidence-based treatment recommendations
for gastroesophageal reflux disease during
pregnancy: A review. Medicine (Baltimore). 2022, Se;
101(35): e30487.
18. Salari N, Mohamadi S, Hemmati M, Fallahi A,
Rasoulpoor S, Zarei H, Shohaimi S, Mohammadi M.
Global prevalence of constipation during pregnancy: a
systematic review and meta-analysis. BMC Pregnancy
Childbirth. 2024, Dec. 24:836
19. Rungsiprakarn P, Laopaiboon M, Sangkomkamhang
US, Lumbiganon P, Pratt JJ. Interventions for treating
constipation in pregnancy. Cochrane Database Syst
Rev. 2015, Sept; (9):CD011448.
20. Poskus T, Sabonyte-Balsaitiene Z, Jakubauskiene L.
et al. Preventing hemorrhoids during pregnancy: a
multicenter, randomized clinical trial. BMC Pregnancy
Childbirth 2022. 22:374.
21. Menees SB, Lembo A, Charabaty A. Fecal Incontinence
and Diarrhea During Pregnancy. Am J Gastroenterol.
2022, Oct; 117: S26-S32.
22. Mahadevan U, Robinson C, Bernasko N, Boland
B, Chambers C, Dubinsky M, Friedman S, Kane S,
Manthey J, Sauberan J, Stones J, Jain R. Inflammatory
Bowel Disease in Pregnancy Clinical Care Pathway:
A Report from the American Gastroenterological
Association IBD Parenthood Project Working Group.
Gastroenterology. 2019, Apr; 156(5): 1508 – 1524.
23. Selinger CP, Nelson-Piercy C, Fraser A, Hall V, Limdi
J, Smith L, Smith M, Nasur R, Gunn M, King A,
Mohan A, Mulgabal K, Kent A, Bel Kok K, Glanville
T. IBD in pregnancy: recent advances, practical management.
Frontline Gastroenterol. 2021; 12(3): 214-
223.
24. Bengtson MB, Aamodt G, Mahadevan U, Vatn MG.
Inadequate Gestational Weight Gain, the Hidden
Link Between Maternal IBD and Adverse Pregnancy
Outcomes: Results from the Norwegian Mother and
Child Cohort Study. Inflamm Bowel Dis. 2017 Jul;
23(7): 1225-1233.
25. Bengston MB, Martin CF, Aamodt G, Morten HV,
Mahadevan U. Inadequate Gestational Weight Gain
Predicts Adverse Pregnancy Outcomes in Mothers
with Inflammatory Bowel Disease: Results from a
Prospective US Pregnancy Cohort. Dig Dis and Sci.
2017; Mar. 62:2063-2069.
26. Hashash JG, Elkin J, Lewis JD, Binion DG. AGA
Clinical Practice Update on Diet and Nutritional
Therapies in Patients with Inflammatory Bowel
Disease: Expert Review. Gastroenterology. 2024 Mar;
166(3): p521-532.
27. Bischoff SC, Bager P, Escher J, Bender DV, Wierdsma
N, Weimann A et al. ESPEN guideline on Clinical
Nutrition in inflammatory bowel disease. Clin Nutr.
2023, Mar; 42(3):352-379.
28. Lamb, CA et al. British Society of Gastroenterology
consensus guidelines on the management of inflammatory
bowel disease in adults. Gut. 2019, Dec; 68(Suppl
3): s1-s106.
29. Ukovic B, Chapman B, Schulberg J, De Cruz P, Choy
MC. Novel Use of the Crohn’s Disease Exclusion Diet
Plus Partial Enteral Nutrition for the Treatment of
Crohn’s Disease During Pregnancy. ACG Case Rep J.
2023; 10: e01078.
30. Yang Q, Tang J, Ding N, Chao K, Li M, Huang Z, Guo
H, Chen J, Zhi M, Hu P, Gao X. Twelve-week peptidebased
formula therapy may be effective in inducing
remission of active Crohn disease among women who
are pregnant or preparing for pregnancy. Nutr Clin
Pract. 2022, Apr; 37(2): 366-376.
31. Moosravi S, Won YM, Wong M, Rezaie A.
Gastroparesis in pregnancy. Am J Obstet Gynecol.
2023, Apr; 228(4):382-394.
32. Camilleri M, Kuo B, Nguyen L, Vaughn VM, Petrey
J, Greer K, Yadlapati R, Abell TL. ACG Clinical
Guideline: Gastroparesis. Am J Gastroenterol. 2022,
Aug; 117(8):1197-1220.
33. Sarkar M, Grab J, Dodgr JL, Gunderson EP, Rubin J,
Irani RA, Cedars M, Terrault N. Non-alcoholic fatty
liver disease in pregnancy is associated with adverse
maternal and perinatal outcomes. J Hepatol. 2020
Sept;73(3):516-522.
34. European Association for the Study of the Liver
(EASL), European Association for the Study of
Diabetes (EASD), and European Association for
the Study of Obesity (EASO). EASL-EASD-EASO
Clinical Practice Guidelines on the management of
metabolic dysfunction-associated steatotic liver disease
(MASLD). J Hepatol. 2024, Sep; 81(3):492-542.
35. Lacy, BE, Pimentel M, Brenner DM, Chey WD,
Keefer LA, Long MD, Moshiree B. ACG Clinical
Guideline: Management of Irritable Bowel Syndrome.
Am J Gastroenterol. 2021; 116(1):17-44.
36. Moosavi S, Pimentel M, Wong M, Rezaie A. Irritable
Bowel Syndrome in Pregnancy. Am J Gastroenterol.
2021; 116:480-490.
37. Lenhart A, Ferch C, Shaw M, Chey WD. Use of
Dietary Management in Irritable Bowel Syndrome:
Results of a Survey of Over 1500 United States
Gastroenterologists. Journal of Neurogastroenterol
Motil. 2018; 24(3): 437-451.

Download Tables, Images & References

A CASE REPORT

Granulomatosis with Polyangiitis Presenting as Crohn’s Disease

March 2025 • Volume XLIX, Issue 3

Read Article

by Eliseo Garcia, Kurt B. Schaberg, Angel A. Herrera Guerra, Arthur J. de Lorimier

Granulomatosis with Polyangiitis (GPA) is a systemic necrotizing vasculitis associated with antineutrophil cytoplasmic antibody (ANCA) that often presents with multiorgan involvement, frequently affecting the upper and lower respiratory tracts and kidneys.1 While bowel involvement can occur, this is rare. Here, we describe a case of GPA with bowel involvement where the endoscopic appearance was like the “skip” lesions one may see in Crohn’s disease (CD) with biopsies confirming the former diagnosis.

Case Presentation

An 11-year-old male presented to the emergency department with anorexia, a 5.48 kg weight loss over the past 5 months, persistent weakness, mouth ulcers, cough, persistent right acute otitis media (AOM), and bilateral testicular pain. His medical history included allergic rhinitis, recurrent AOM, malnutrition, and right epididymitis. Over the past two months, he exhibited a normal bowel pattern, but experienced increasing fatigue and weakness, decreased oral intake, and intermittent abdominal pain.

His physical exam revealed a cachectic adolescent with unexpected weight loss who weighed 21.82 kg (0.01 percentile); physical exam also demonstrated a purulent effusion in the right ear and a serous effusion in the left ear. Laboratory results exhibited normocytic anemia (Hgb 9.6 g/dL, MCV 85.1 fl), elevated inflammatory markers (WBC 17.7 K/mm3, ESR 62 mm/hr, CRP 10.6 mg/dL, calprotectin 1690 ug/g), elevated eosinophils (0.8 K/mm3), and a positive c-ANCA pattern with a high ANCA IFA titer (>1:1280). Nasal endoscopy revealed significant scarring and stenosis of the bilateral nasal cavities with minimal nasal patency. CT of the head and sinus revealed pansinusitis sequelae, while chest X-rays and CT demonstrated perihilar opacities and bilateral perihilar infiltrates/masses with necrotic foci, respectively. On upper endoscopy, two large esophageal ulcers were visualized adjacent to one another with biopsies showing normal surrounding mucosa. Colonoscopy revealed aphthous lesions reminiscent of “skip” lesions in the ascending and transverse colon (Figure 1). Colon biopsies demonstrated submucosal vasculitis with associated poorly formed granulomas that lacked cryptitis (ie. inflammation that did not span the entire mucosal width) (Figure 2). There were also areas of fibrinopurulent exudate consistent with ulceration throughout the gastrointestinal tract and ischemic changes in the duodenum. 

Based on these findings, the patient was diagnosed with granulomatosis with polyangiitis and treated with a methylprednisolone pulse (22 mg/kg on day one followed by 17.5 mg/kg after two days), three doses of rituximab (375 mg/m2 at approximately one-week intervals), and an oral prednisolone taper (20 mg BID for seven days, weaned down to 25 mg once daily). 

In subsequent follow up over a 6-month period, the patient demonstrated signs of clinical improvement, with resolution of anemia, normal inflammatory markers (i.e. ESR, CRP, and calprotectin), and a weight gain of 12.8 kg (22nd percentile); the patient continues to receive appropriate follow up care.

Discussion

This case explores a unique situation where GPA, previously Wegener’s granulomatosis, manifested similarly to CD. CD is a chronic inflammatory bowel disease characterized by full-thickness inflammation of the bowel that impairs the lining of the digestive tract and can lead to abdominal pain, diarrhea, fatigue, weight loss, and malnutrition.2 Of importance, CD may also present with various extraintestinal manifestations, including respiratory tract involvement, although this is uncommon.3

In our patient’s case, the presentation was primarily gastrointestinal, characterized by symptoms such as decreased oral intake, early satiety, intermittent abdominal pain, and weight loss, which are more commonly associated with CD.2 Histologically, the colon biopsies most prominently showed submucosal changes, including vasculitis and granulomas with what appeared to be secondary mucosal changes like ischemia and erosion (Figure 2). This contrasts with the transmural mucosal acute and chronic inflammation characteristic of inflammatory bowel disease. Additionally, laboratory results revealed normocytic anemia, elevated inflammatory markers, elevated eosinophils, and a positive c-ANCA pattern with a high ANCA IFA titer, indicative of GPA.1

While there have been reports of GPA with gastrointestinal symptoms similar to CD,3,4 the occurrence of such symptoms is relatively low, being described in about 10-24% of GPA patients.4 When juxtaposed with previous studies, our patient’s presentation is distinct because our case involves a pediatric patient with both systemic and significant gastrointestinal symptoms,3,4 which is highly atypical in a pediatric population, with an occurrence of GPA in this population being 1:1,000,000.5 Furthermore, the presence of CD or GPA manifesting as a mimic of the other condition has generally only been reported in adults (two previously published case reports with patients aged 29 and 41),6,7 potentially making this case, to the best of our knowledge, the second instance of a pediatric patient who’s diagnosed GPA presents as CD without also having a concurrent diagnosis of CD.8

Conclusion

In conclusion, this case underscores the importance of considering GPA in the differential diagnosis when a patient presents with gastrointestinal symptoms akin to CD, especially when accompanied by systemic symptoms, respiratory symptoms, and a positive c-ANCA pattern.3,4 Further research is warranted to understand the relationship between GPA and CD and to enhance the diagnosis and treatment of these conditions. 

References

1. Csernok E, Gross WL. Current understanding of the pathogenesis of
granulomatosis with polyangiitis (Wegener’s). Expert Rev Clin Immunol.
2013;9(7):641-648. doi:10.1586/1744666X.2013.811052
2. Dolinger M, Torres J, Vermeire S. Crohn’s disease. Lancet. Published
online March 1, 2024:S0140-6736(23)02586-2. doi:10.1016/S0140-
6736(23)02586-2
3. Vaszar LT, Orzechowski NM, Specks U, et al. Coexistent pulmonary granulomatosis
with polyangiitis (Wegener granulomatosis) and Crohn disease. Am
J Surg Pathol. 2014;38(3):354-359. doi:10.1097/PAS.0000000000000135
4. Jóźwiak L, Ławnicka I, Książek A. Coexistence of granulomatosis with polyangiitis
(GPA) and Crohn’s disease or multiorgan manifestation of the same
disease? Reumatologia. 2016;54(2):86-90. doi:10.5114/reum.2016.60219
5. Bohm M, Gonzalez Fernandez MI, Ozen S, et al. Clinical features of childhood
granulomatosis with polyangiitis (wegener’s granulomatosis). Pediatr
Rheumatol Online J. 2014;12:18. doi:10.1186/1546-0096-12-18
6. Sinnott JD, Matthews P, Fletcher S. Colitis: an unusual presentation of
Wegener’s granulomatosis. BMJ Case Rep. 2013;2013:bcr2012007566.
doi:10.1136/bcr-2012-007566
7. Schneider A, Menzel J, Gaubitz M, Keller R, Lügering N, Domschke W.
Colitis as the initital presentation of Wegener’s granulomatosis. Journal of
Internal Medicine. 1997;242(6):513-517. doi:10.1111/j.1365-2796.1997.
tb00025.x
8. Sokol RJ, Farrell MK, McAdams AJ. An unusual presentation of Wegener’s
granulomatosis mimicking inflammatory bowel disease. Gastroenterology.
1984;87(2):426-432. doi:10.1016/0016-5085(84)90724-8

Download Tables, Images & References

Dispatches from the GUILD Conference, Series #66

Diagnosis and Managementof Gastroparesis

March 2025 • Volume XLIX, Issue 3
Michael Camilleri

Read Article

This review appraises the symptoms associated with gastroparesis and the optimal measurement to identify delayed gastric emptying. The diagnosis requires differentiation from functional dyspepsia, iatrogenic disease (e.g., opiates and GLP-1 agonists), and conditions associated with vomiting including rumination and cannabinoid hyperemesis. Management includes normalization of hydration and nutrition and relief of symptoms which typically requires pharmacological treatment predominantly with prokinetics and antiemetics. Metoclopramide is the only FDA-approved medication for treatment of gastroparesis, but there are restrictions for its use. Targeting the fundus and visceral sensation may also provide symptom relief. Treatment of abnormal pyloric contractility or poor distensibility may be targeted with intra-pyloric botulinum toxin injection or, increasingly in practice, gastric per-oral endoscopic myotomy. This is increasingly applied for patients not responding to dietary and pharmacological approaches. There is significant unmet need in the treatment of gastroparesis.

Introduction

The overall objectives are to review the definition, optimal measurement of gastric emptying (GE) of solids, and differential diagnosis and management of gastroparesis. It is important to distinguish between gastroparesis and functional dyspepsia which affects about 8% of people in the community in 26 countries,1 whereas definite gastroparesis (symptoms plus delayed gastric emptying) is reported in 13.8 to 267.7 per 100,000 adults.2,3 

Definition

Gastroparesis is identified in clinical practice through recognition of the clinical symptoms and documentation of delayed GE in the absence of gastric outlet obstruction. Symptoms resulting from gastroparesis include nausea, vomiting, early satiety, postprandial fullness, bloating, and upper abdominal pain.4

Diagnosis

A sine qua non for diagnosis of gastroparesis is an accurate, reliable assessment of emptying of solid, digestible food, appraisal for at least 3 and preferably 4 hours, robust normative data, and reproducibility. This excludes radiopaque markers and wireless motility capsule (not digestible), water or nutrient liquids as food substrates. Three available tests (2 scintigraphic and 1 stable isotope) are approved: 

a. The egg-substitute 250kcal with 2% fat Eggbeaters® meal is the most widely used; the cut-off for delayed GE is >60% retention at 2 hours, and >10% retained at 4h,5 based on 95th percentile of a study of 123 healthy volunteers.6 This meal has an emptying profile almost identical to that of the liquid nutrient meal, Ensure.®7 Moreover, the reproducibility on replicate testing 48 weeks apart was ~40%.8

b. The Mayo two scrambled real egg meal (320kcal, 30% fat) has reproducibility rate of >80%,9 with 95%ile of GE T1/2 >174min; GE at 2h <25% emptied; GE at 4h <75% emptied, based on 319 healthy controls.10

c. The 13C-spirulina stable isotope breath test using reconstituted real egg 238kcal, 42% fat meal, was validated with simultaneous scintigraphy,11 and effects of pharmacological acceleration and delay of GE.12

Other tests infrequently used in the diagnosis of gastroparesis are antropyloroduodenal manometry (to diagnose antral hypomotility,13 pylorospasm,14 differentiate neuropathy from myopathy based on amplitude of contractions15), or EndoFLIP of the pylorus (to identify pyloric diameter and distensibility16,17). 

Gastrointestinal symptoms such as nausea or vomiting are significantly correlated with GE measured optimally (solid meal over >3h)18 based on a systematic review and meta-analysis.19  

Differential Diagnosis

The main considerations are functional dyspepsia (differentiation based on a reliable GE test), rumination syndrome (predominantly through classical effortless regurgitation within 20 minutes after every meal20,21), cyclic vomiting or cannabinoid hyperemesis syndrome (CHS) and iatrogenic disease (predominantly GLP-1 receptor agonists22,23, opiates24, tetrahydrocannabinol25, and cannabidiol26). CHS is associated with chronic (typically years) and heavy (typically daily or near-daily) cannabis use and predominance in males.27 

Management

Management of gastroparesis should include correction of nutritional state, relief of symptoms, improvement of GE and glycemic control in those with diabetes,28 and identifying and treating the underlying pathophysiology.

A. Hydration and nutrition

When patients with gastroparesis have significant fluid or metabolic derangements (e.g., ketoacidosis, renal insufficiency, hyperglycemia) due to nausea and vomiting or underlying metabolic diseases such as diabetes, restoration of hydration and electrolyte balance (especially K+, Ca++, Mg++) is essential through per-oral or intravenous routes.29  

Nutritional deficiencies are highly prevalent among patients with gastroparesis; up to 64% of patients with gastroparesis consume <60% of the estimated total kcal needs, and vitamin (A, B6, C, K) and mineral (iron, potassium, zinc) deficiencies are common.30

The first dietary modifications, that is, homogenizing solids to smaller particle size, reducing fat, and cooking of nondigestible fibers, reduced the severity of nausea, vomiting, postprandial fullness, bloating, and regurgitation/heartburn in patients with diabetic gastroparesis.31 If these are not tolerated, stepwise nutritional interventions include liquid meals, oral nutrition supplements, enteral nutrition, and parenteral nutrition.32 Enteral feeding should be directly into the jejunum, rather than via jejunal extension from gastrostomy tube; it is safe and leads to weight regain.33 Parenteral nutrition is used temporarily for severe nutritional deficiency, is rarely required long term in those with intolerance of jejunal feeding, and it may be associated with complications such as infections and thromboses.34  

B. Pharmacologic agents

Figure 1. shows a conceptual summary of pharmacological approaches to treat gastroparesis directed at vomiting center receptors and neurons in the enteric nervous system.

B. i. Prokinetics

The 2022 gastroparesis guideline35 recommended therapies that target GE and symptoms of idiopathic and diabetic gastroparesis, while weighing the benefits and risks of the agent. Prokinetic agents enhance GE and reduce symptoms. In a systematic review of randomized, blinded, parallel, or crossover trials with optimal GE tests, meta-regression showed a positive association between accelerated GE T1/2 by at least 20.4 minutes and upper gastrointestinal symptoms.19 This conclusion was independently confirmed.36  

B. ii. Dopaminergic modulation

Metoclopramide approved by FDA for gastroparesis in 1979, functions through antagonism of central and peripheral dopamine receptors. Central antiemetic effects are mediated by inhibition of dopamine D2 and 5-HT3 receptors in the area postrema (vomiting center), located outside the blood–brain barrier and a target of several antiemetics.37 Peripherally, metoclopramide exerts prokinetic effects through agonism on 5-HT4 receptors on cholinergic neurons and antagonism of D2 receptor.38 Metoclopramide crosses the blood-brain barrier and can cause anxiety, agitation, somnolence, and reversible extrapyramidal symptoms including tremors. In 1 in 1000-10,000 patients, irreversible tardive dyskinesia occurred.39,40 Because of risk of neurological adverse effects, metoclopramide is only approved for a maximum of 12 weeks and carries a black box warning. 

Routes of administration are oral (tablet or liquid preparation), nasal spray,41 and parenteral (e.g., i.v. or subcutaneous) formulations.42 As the only approved medication for gastroparesis, practitioners should prescribe lowest effective dose of liquid, nasal, or tablet formulation, 5-10 mg t.i.d. 15 minutes before meals for 12 weeks. If tolerated, there should be “drug holidays” between prescription cycles, with symptomatic remedies such as liquid or blenderized diet, antiemetic agents (e.g., ondansetron 4-8 mg b.i.d.), or short-term (to avoid tachyphylaxis) erythromycin, 40-200 mg t.i.d. as tolerated.43 

B. iii.
Other marketed agents used off-label in gastroparesis

Other marketed agents used off-label include domperidone, macrolides, and 5-HT4 receptor agonists such as cisapride and prucalopride.

B. iii. a. Domperidone 

Domperidone is a peripherally acting dopamine D2 receptor antagonist that is available through the FDA’s Program for Expanded Access to Investigational Drugs. The recommended dose of domperidone is 10-20 mg t.i.d. at bedtime. Its efficacy for the treatment of gastroparesis is comparable to metoclopramide.44 A systematic review of 28 trials showed symptomatic reduction (64%), decreased hospitalization (67%), and accelerated GE (60% of the studies).45 Domperidone does not cross the blood-brain barrier. Domperidone was associated with corrected QT interval (QTc) prolongation, and it should be avoided in patients with prolonged QTc (>470 ms in males, >450 ms in females).46

B. iii. b. Motilin agonists

Macrolides such as erythromycin, azithromycin, and clarithromycin are motilin receptor agonists with a prokinetic property. In a systematic review of 5 small-scaled, short-term studies, erythromycin accelerated gastric emptying and improved symptoms in 43% of patients with gastroparesis.47 Oral erythromycin is associated with tachyphylaxis within days to weeks due to down-regulation of the motilin receptor.48 Although erythromycin may prolong the QTc, a systematic review and network meta-analysis of 33 studies (22.6 million subjects) found no association with risk of arrhythmia or cardiovascular mortality.49

There are no randomized, placebo-controlled trials of azithromycin and clarithromycin to assess efficacy of symptoms in patients with gastroparesis.

B. iii. c. 5-HT4 agonists used off-label

Prucalopride is highly selective for 5-HT4 receptors. Two available randomized, placebo-controlled, cross-over trials of prucalopride in gastroparesis50,51 showed greater benefit in patients with idiopathic gastroparesis than in gastroparesis secondary to underlying diseases (diabetes or connective tissue diseases).

Cisapride accelerated GE and improved symptoms in placebo-controlled trials conducted in short-term or medium-term trials (e.g., 6- or 8-week duration) in gastroparesis.35 Cisapride is a potent inhibitor of the human ether-à-go-go-related gene (hERG) potassium channel and with reports, extremely rarely, of cardiac arrhythmias. It is also only available for compassionate use in selected cases in the USA. 

B. III. d. Cholinesterase inhibitors used off-label for gastroparesis

Neostigmine is a short-acting (15-30min) parenteral acetylcholinesterase (ACE) inhibitor that induces fasting gastroduodenal motor activity,52 accelerates GE of liquids in critically ill patients with delayed GE,53 and should only be used in hospital, as it induces vagotonia and bradycardia; EKG monitoring and atropine 0.6-1.2mg should be available while neostigmine is administered. 

Pyridostigmine has longer duration of action (4h), is available as liquid or tablet, and is prescribed at a dose of 60mg t.i.d. In an open-label series in children with gastrointestinal dysmotilities, pyridostigmine was beneficial in relief of symptoms.54  

B. III. e. Ghrelin receptor agonist

Ghrelin is a 28-amino acid orexigenic hormone found primarily in the stomach. A pharmacological dose of ghrelin increased proximal gastric tone through central and peripheral effects.55 Relamorelin, a pentapeptide ghrelin receptor agonist, increased the frequency of distal antral contractions without inhibiting gastric accommodation or inducing satiation.56 

Relamorelin had proven clinical efficacy and safety in phase 2A and 2B, randomized, controlled trials in patients with diabetic gastroparesis but not in subsequent phase III trials.57

C. Antiemetics

C. i. 5-HT3 antagonists

Ondansetron targets stomach distention, alleviating nausea without affecting gastric compliance, volume, or accommodation.58 Ondansetron is available as oral tablet, oral dissolution, and intravenous formulations, and is dosed at 4-8mg every 8 hours as needed. Ondansetron can cause QTc prolongation and rarely cardiac arrhythmia. Baseline EKG is recommended. Granisetron is also available orally and i.v., and the sustained release transdermal patch of granisetron significantly improved nausea and vomiting in an open-label study of 51 patients with gastroparesis.59 Tropisetron, effective for cancer or chemotherapy-induced nausea and vomiting, has potential in gastroparesis based on a dog study.60

Constipation is a known adverse effect of this class of medications.

C. ii. Agents targeting multiple receptors

Prochlorperazine is primarily a D2 receptor antagonist, with ability to block histaminergic, cholinergic, and noradrenergic receptors. Promethazine primarily acts as an antagonist for histamine receptors (H1), with additional antagonism at dopamine, adrenergic, N-methyl-D-aspartate, and muscarinic cholinergic receptors. 

Scopolamine competes for binding at muscarinic (M1) receptors, inhibiting cholinergic nerve stimulation. 

All these antiemetics are available in orally disintegrating tablets, dermal, or rectal formulations for patients with gastroparesis. Cholinergic side effects like sedation, dry mouth, and constipation are frequent. Promethazine may be habit forming and is reserved as a “rescue” agent.

Mirtazapine acts on several receptors: presynaptic α2 adrenergic receptors, several 5-HT receptor subtypes, and H1 receptor. Agonist effects on central and peripheral 5-HT1A receptors influence gastric receptive fundic relaxation. In a 4-week trial in gastroparesis, mirtazapine improved nausea, vomiting, retching, loss of appetite, and patient grading assessment compared with pretreatment.61

C. iii. Neurokinin-1 antagonists

Aprepitant (approved for chemotherapy-induced emesis) affects the vomiting center in the brainstem and enhances gastric accommodation without slowing GE.62 In a randomized, double-blind, placebo-controlled trial of 126 patients with chronic nausea and vomiting of presumed gastric origin, aprepitant, 125mg daily, significantly reduced severity of nausea, vomiting, and overall symptoms.63  

Tradipitant is an investigational agent which was demonstrated to decrease nausea score, increase nausea-free days, and improve the GCSI score in patients with gastroparesis compared to placebo.64 Benefit was documented when controlling for drug exposure, rescue medications, and baseline severity inflation.65  

C. iv. Cannabinoid agents

The primary ingredient in marijuana is tetrahydrocannabinol (THC), a nonselective cannabinoid receptor agonist. Although THC delays gastric emptying of solids,66 a database of 506 patients with gastroparesis, showed 12% used medical or recreational marijuana for symptomatic relief.67  

Cannabidiol (CBD), a low-THC extract from Cannabis sativa approved for seizure disorders, blocks CBR1 and CBR2 receptors. CBD twice daily (Epidiolex® escalated to 20mg/kg/d) in 44 patients68 was efficacious in gastroparesis, with reduction in total GCSI score, ability to finish a normal-sized meal, vomiting, and overall symptom severity, despite slower GE of solids. CBD’s effectiveness was attributed to anxiolytic and visceral analgesic properties.69  

D. Neuromodulators for pain relief

Patients frequently experience abdominal pain with gastroparesis; however, those primarily presenting with abdominal pain should be evaluated for alternative diagnoses. In a randomized trial involving 130 patients diagnosed with idiopathic gastroparesis, nortriptyline did not demonstrate superiority over placebo in alleviating symptoms, as measured by the GCSI score.70 

E. Targeting the fundus 

About  20%  of   284 patients with proven  gastroparesis have increased gastric accommodation.71 Erythromycin (motilin and cholinergic receptor agonism) stimulates both fundic contraction and antral motor function and accelerates GE.72,73 Erythromycin was tested in an open-labeled study: at 4 weeks, there was acceleration of GE and reduced symptoms, but efficacy was lost over time,74 reflecting tachyphylaxis.48

For dyspeptic symptoms with both reduced GE and reduced accommodation,75 buspirone, a 5-HT1A agonist with anxiolytic properties, improved aggregate symptoms and nausea in response to a nutrient challenge meal in healthy controls.76 On the other hand, patients with moderate-to-severe early satiety or postprandial fullness and other symptoms of gastroparesis did not benefit from treatment with buspirone.77   

Although mirtazapine has 5-HT1A effects, the improvements in nausea, vomiting, retching, and loss of appetite61 appear unrelated to alteration in gastric accommodation.78  

F. Targeting the pylorus

In a subset of patients with gastroparesis, pyloric dysfunction, characterized by abnormally prolonged and intense tonic contractions of the pylorus, was noted.14 After excluding iatrogenic dysfunction (e.g. opiates),24 open-label studies showed intrapyloric injection of botulinum toxin had short-term (<6 months) efficacy in accelerating GE and improving symptoms.79 However, two randomized, placebo-controlled trials did not confirm efficacy in achieving symptom improvement.80,81 Measurements of pyloric diameter and distensibility index may predict response to therapy, particularly post–G-POEM (discussed below)82 or after botulinum toxin injection for relief of vomiting.83  

G. Electrical approaches 

Gastric electric stimulation (GES) may be considered for control of gastroparesis symptoms as a humanitarian use device. Randomized, crossover trials of gastric electric stimulation have shown mixed results, sometimes with improvement in symptoms but no differences in gastrointestinal quality of life, nutritional parameters, or GE, suggesting possible effects on visceral afferents rather than the motor function of stomach (trials reviewed elsewhere35).

H. Endoscopic or surgical approaches 

In patients with gastroparesis with symptoms refractory to medical therapy, pyloromyotomy (nowadays almost exclusively through G-POEM) is recommended over no treatment for symptom control,35 based predominantly on open-label studies. One sham-controlled study of 6 months’ duration documented relief of symptoms and improved GE with G-POEM procedure.84  

In 177 patients with gastroparesis, laparoscopic pyloroplasty improved GE in 90% of patients and induced short-term improvement of nausea, vomiting, bloating, and abdominal pain. However, morbidity rate was 6.8%, including leaks requiring further surgery.85

Conclusion

A careful appraisal of symptoms is necessary in suspected gastroparesis: “If patient has predominant pain, think again”. A solid GE test is essential. Normalization of hydration and nutrition, and relief of symptoms typically requires pharmacological treatment. G-POEM is increasingly applied for patients not responding to dietary and pharmacological approaches. 

References

1. Sperber AD, Bangdiwala SI, Drossman DA, et al. Worldwide prevalence and burden of functional gastrointestinal disorders, results of Rome foundation global study. Gastroenterology 2021;160:99-114.

2. Dilmaghani S, Zheng T, Camilleri M. Epidemiology and healthcare utilization in patients with gastroparesis: a systematic review. Clin Gastroenterol Hepatol 2023;21:2239–2251.e2.

3. Ye Y, Yin Y, Huh SY, Almansa C, Bennett D, Camilleri M. Epidemiology, etiology, and treatment of gastroparesis: real-world evidence from a large US national claims database. Gastroenterology 2022;162:109-121.e5. 

4. Camilleri M, Parkman H, Shafi M, Abell T, Gerson L, American College of Gastroenterology. Clinical guideline: management of gastroparesis. Am J Gastroenterol 2013;108:18-37.

5. Maurer AH, Camilleri M, Donohoe K, et al. The SNMMI and EANM practice guideline for small-bowel and colon transit 1.0. J Nucl Med 2013;54:2004-2013. 

6. Tougas G, Eaker EY, Abell TL, et al. Assessment of gastric emptying using a low fat meal: establishment of international control values. Am J Gastroenterol 2000;95:1456-1462.

7. Sachdeva P, Kantor S, Knight LC, Maurer AH, Fisher RS, Parkman HP. Use of a high caloric liquid meal as an alternative to a solid meal for gastric emptying scintigraphy. Dig Dis Sci 2013;58:2001-2006.

8. Pasricha PJ, Grover M, Yates KP, et al. Functional dyspepsia and gastroparesis in tertiary care are interchangeable syndromes with common clinical and pathologic features. Gastroenterology 2021;160:2006-2017.

9. Camilleri M, Zheng T, Vosoughi K, Lupianez-Merly C, Eckert D, Busciglio I, Burton D, Dilmaghani S. Optimal measurement of gastric emptying of solids in gastroparesis or functional dyspepsia: evidence to establish standard test. Gut 2023;72:2241-2249.

10. Camilleri M, Iturrino J, Bharucha AE, Burton D, Shin A, Jeong I-D, Zinsmeister AR. Performance characteristics of scintigraphic measurement of gastric emptying of solids in healthy participants. Neurogastroenterol Motil 2012;24:1076–e562.

11. Szarka LA, Camilleri M, Vella A, Burton D, Baxter K, Simonson J, Zinsmeister AR. A stable isotope breath test with a standard meal for abnormal gastric emptying of solids in the clinic and in research. Clin Gastroenterol Hepatol 2008;6:635-643.

12. Viramontes BE, Kim DY, Camilleri M, Lee JS, Stephens D, Burton DD, Thomforde GM, Klein PD, Zinsmeister AR. Validation of a stable isotope gastric emptying test for normal, accelerated or delayed gastric emptying. Neurogastroenterol Motil 2001;13:567-574.

13. Camilleri M, Malagelada J-R, Stanghellini V, Fealey RD, Sheps SG. Gastrointestinal motility disturbances in patients with orthostatic hypotension. Gastroenterology 1985;88:1852-1859.

14. Mearin F, Camilleri M, Malagelada J-R. Pyloric dysfunction in diabetics with recurrent nausea and vomiting. Gastroenterology 1986;90:1919-1925.

15. Thumshirn M, Bruninga K, Camilleri M. Simplifying the evaluation of postprandial antral motor function in patients with suspected gastroparesis. Am J Gastroenterol 1997;92:1496-1500.

16. Malik Z, Sankineni A, Parkman HP. Assessing pyloric sphincter pathophysiology using EndoFLIP in patients with gastroparesis. Neurogastroenterol Motil 2015;27:524-531.

17.  Desprez C, Chambaz M, Melchior C, Basile P, Prevost G, Jacques J, Leroi AM, Gourcerol G. Assessment of pyloric sphincter distensibility and pressure in patients with diabetic gastroparesis. Neurogastroenterol Motil 2021;33:e14064.

18. Vijayvargiya P, Jameie-Oskooei S, Camilleri M, Chedid V, Erwin PJ, Murad MH. Association between delayed gastric emptying and upper gastrointestinal symptoms: a systematic review and meta-analysis. Gut 2019;68:804-813.

19. Vijayvargiya P, Camilleri M, Chedid V, Mandawat A, Erwin PJ, Murad MH. Effects of promotility agents on gastric emptying and symptoms: a systematic review and meta-analysis. Gastroenterology 2019;156:1650-1660.

20. O’Brien MD, Bruce BK, Camilleri M. The rumination syndrome: clinical features rather than manometric diagnosis. Gastroenterology 1995;108:1024-1029. 

21. Chial HJ, Camilleri M, Williams DE, Litzinger K, Perrault J. Rumination syndrome in children and adolescents: diagnosis, treatment, and prognosis. Pediatrics 2003;111:158-162.

22. Camilleri M, Lupianez-Merly C. Effects of GLP-1 and other gut hormone receptors on the gastrointestinal tract and implications in clinical practice. Am J Gastroenterol 2024;119:1028-1037. 

23. Camilleri M, Carlson P, Dilmaghani S. Prevalence and variations in gastric emptying delay in response to GLP-1 receptor agonist liraglutide. Obesity (Silver Spring). 2024;32:232-233. 

24. Camilleri M, Sanders KM. Opiates, the pylorus, and gastroparesis. Gastroenterology 2020;159:414-421.

25. McCallum RW, Soykan I, Sridhar KR, Ricci DA, Lange RC, Plankey MW. Delta-9-tetrahydrocannabinol delays the gastric emptying of solid food in humans: a double-blind, randomized study. Aliment Pharmacol Ther 1999;13:77-80. 

26. Jehangir A, Parkman HP. Cannabinoid use in patients with gastroparesis and related disorders: prevalence and benefit. Am J Gastroenterol 2019;114:945-953.  

27.  Rubio-Tapia A, McCallum R, Camilleri M. AGA clinical practice update on diagnosis and management of cannabinoid hyperemesis syndrome: commentary. Gastroenterology 2024;166:930-934.   

28. Camilleri M, Parkman HP, Shafi MA, Abell TL, Gerson L, American College of Gastroenterology. Clinical guideline: management of gastroparesis. Am J Gastroenterol 2013;108:18-37.

29. Camilleri M. Diabetic gastroparesis. New Engl J Med 2007;356:820-829.

30. Parkman HP, Yates KP, Hasler WL, Nguyen L, Pasricha PJ, Snape WJ, Farrugia G, Calles J, Koch KL, Abell TL, McCallum RW, Petito D, Rees Parrish C, Duffy F, Lee L, Unalp-Arida A, Tonascia J, Hamilton F, NIDDK Gastroparesis Clinical Research Consortium. Dietary intake and nutritional deficiencies in patients with diabetic or idiopathic gastroparesis. Gastroenterology 2011;141:486-498.e1-e7.

31. Olausson EA, Storsrud S, Grundin H, Isaksson M, Attvall S, Simren M. A small particle size diet reduces upper gastrointestinal symptoms in patients with diabetic gastroparesis: a randomized controlled trial. Am J Gastroenterol 2014;109:375-385.

32. Limketkai BN, LeBrett W, Lin L, Shah ND. Nutritional approaches for gastroparesis. Lancet Gastroenterol Hepatol 2020;5:1017-1026.

33. Fontana RJ, Barnett JL. Jejunostomy tube placement in refractory diabetic gastroparesis: a retrospective review. Am J Gastroenterol 1996;91:2174-2178.

34. Bharadwaj S, Meka K, Tandon P, Rathur A, Rivas JM, Vallabh H, Jevenn A, Guirguis J, Sunesara I, Nischnick A, Ukleja A. Management of gastroparesis-associated malnutrition. J Dig Dis 2016;17:285-294.

35. Camilleri M, Kuo B, Nguyen L, Vaughn VM, Petrey J, Greer K, Yadlapati R, Abell TL. ACG Clinical Guideline: Gastroparesis. Am J Gastroenterol 2022;117:1197-1220.

36. Goelen N, Jones M, Huang IH, Carbone F, Janssen P, Tack J. Do prokinetic agents provide symptom relief through acceleration of gastric emptying? An update and revision of the existing evidence. United European Gastroenterol J 2023;11:146-162.

37. Sanger GJ. Translating 5-HT4 receptor pharmacology. Neurogastroenterol Motil 2009;21:1235-1238.

38. Tonini M, Cipollina L, Poluzzi E, et al. Review article: clinical implications of enteric and central D2 receptor blockade by antidopaminergic gastrointestinal prokinetics. Aliment Pharmacol Ther 2004;19:379-390.

39. Rao AS, Camilleri M. Review article: metoclopramide and tardive dyskinesia. Aliment Pharmacol Ther 2010;31:11-19. 

40. Al-Saffar A, Lennernas H, Hellstrom PM. Gastroparesis, metoclopramide, and tardive dyskinesia: Risk revisited. Neurogastroenterol Motil 2019;31:e13617.

41. Parkman HP, Carlson MR, Gonyer D. Metoclopramide nasal spray reduces symptoms of gastroparesis in women, but not men, with diabetes: results of a phase 2b randomized study. Clin Gastroenterol Hepatol 2015;13:1256-1263.e1251.

42. McCallum RW, Valenzuela G, Polepalle S, Spyker D. Subcutaneous metoclopramide in the treatment of symptomatic gastroparesis: clinical efficacy and pharmacokinetics. J Pharmacol Exp Ther 1991;258:136-142.

43. Camilleri M. Beyond metoclopramide for gastroparesis. Clin Gastroenterol Hepatol 2022;20:19-24.

44. Patterson D, Abell T, Rothstein R, Koch K, Barnett J. A double-blind multicenter comparison of domperidone and metoclopramide in the treatment of diabetic patients with symptoms of gastroparesis. Am J Gastroenterol 1999;94:1230-1234. 

45. Sugumar A, Singh A, Pasricha PJ. A systematic review of the efficacy of domperidone for the treatment of diabetic gastroparesis. Clin Gastroenterol Hepatol 2008;6:726-733.

46. Dumitrascu DL, Weinbeck M. Domperidone versus metoclopramide in the treatment of diabetic gastroparesis. Am J Gastroenterol 2000;95:316-317.

47. Maganti K, Onyemere K, Jones MP. Oral erythromycin and symptomatic relief of gastroparesis: a systematic review. Am J Gastroenterol 2003;98:259-263.

48. Thielemans L, Depoortere I, Perret J, Robberecht P, Liu Y, Thijs T, Carreras C, Burgeon E, Peeters TL. Desensitization of the human motilin receptor by motilides. J Pharmacol Exp Ther 2005;313:1397-1405.

49. Gorelik E, Masarwa R, Perlman A, Rotshild V, Muszkat M, Matok I. Systematic review, meta-analysis, and network meta-analysis of the cardiovascular safety of macrolides. Antimicrob Agents Chemother 2018;62:e00438-e00518.

50. Carbone F, Van den Houte K, Clevers E, Andrews CN, Papathanasopoulos A, Holvoet L, Van Oudenhove L, Caenepeel P, Arts J, Vanuytsel T, Tack J. Prucalopride in gastroparesis: a randomized placebo-controlled crossover study. Am J Gastroenterol 2019;114:1265-1274. 

51. Andrews CN, Woo M, Buresi M, Curley M, Gupta M, Tack J, Wilsack L, Nasser Y. Prucalopride in diabetic and connective tissue disease-related gastroparesis: Randomized placebo-controlled crossover pilot trial. Neurogastroenterol Motil 2021;33:e13958.

52. Bortolotti M, Cucchiara S, Sarti P, Brunelli F, Mazza M, Bagnato F, Barbara L. Comparison between the effects of neostigmine and ranitidine on interdigestive gastroduodenal motility of patients with gastroparesis. Digestion 1995;56:96-99.

53. Lucey MA, Patil V, Girling K, Jacques T, O’Leary M. Does neostigmine increase gastric emptying in the critically ill-results of a pilot study. Crit Care Resusc 2003;5:14-19.

54. Manini ML, Camilleri M, Grothe R, Di Lorenzo C. Application of pyridostigmine in pediatric gastrointestinal motility disorders: a case series. Pediatr Drugs 2017;20:173-180. 

55. Peeters TL. Central and peripheral mechanisms by which ghrelin regulates gut motility. J Physiol Pharmacol 2003;54(Suppl 4):95-103.  

56. Nelson AD, Camilleri M, Acosta A, Busciglio I, Linker Nord S, Boldingh A, Rhoten D, Ryks M, Burton D. Effects of ghrelin receptor agonist, relamorelin, on gastric motor functions and satiation in healthy volunteers. Neurogastroenterol Motil 2016;28:1705-1713.

57. Camilleri M, Jencks KJ. Pharmacological treatments for gastroparesis. Pharmacological Reviews (2025, in press).

58. Janssen P, Vos R, Van Oudenhove L, Tack J. Influence of the 5-HT3 receptor antagonist ondansetron on gastric sensorimotor function and nutrient tolerance in healthy volunteers.  Neurogastroenterol Motil 2011;23:444-449, e175.  

59. Midani D, Parkman HP. Granisetron transdermal system for treatment of symptoms of gastroparesis: a prescription registry study. J Neurogastroenterol Motil 2016;22:650-655.

60. Gullikson GW, Loeffler RF, Viriña MA. Relationship of serotonin-3 receptor antagonist activity to gastric emptying and motor-stimulating actions of prokinetic drugs in dogs. J Pharmacol Exp Ther 1991;258:103-110.

61. Malamood M, Roberts A, Kataria R, Parkman HP, Schey R. Mirtazapine for symptom control in refractory gastroparesis. Drug Des Devel Ther 2017;11:1035-1041.

62. Jacob D, Busciglio I, Burton D, Halawi H, Oduyebo I, Rhoten D, Ryks M, Harmsen WS, Camilleri M. Effects of NK1 receptors on gastric motor functions and satiation in healthy humans: results from a controlled trial with the NK1 antagonist aprepitant. Am J Physiol Gastrointest Liver Physiol 2017;313:G505-G510.

63. Pasricha PJ, Yates KP, Sarosiek I, McCallum RW, Abell TL, Koch KL, Nguyen LAB, Snape WJ, Hasler WL, Clarke JO, Dhalla S, Stein EM, Lee LA, Miriel LA, Van Natta ML, Grover M, Farrugia G, Tonascia J, Hamilton FA, Parkman HP, NIDDK Gastroparesis Clinical Research Consortium (GpCRC). Aprepitant has mixed effects on nausea and reduces other symptoms in patients with gastroparesis and related disorders. Gastroenterology 2018;154:65-76.e11.

64. Carlin JL, Lieberman VR, Dahal A, Keefe MS, Xiao C, Birznieks G, Abell TL, Lembo A, Parkman HP, Polymeropoulos MH. Efficacy and safety of tradipitant in patients with diabetic and idiopathic gastroparesis in a randomized, placebo-controlled trial. Gastroenterology 2021;160:76-87.e74.

65. Carlin JL, Polymeropoulos C, Camilleri M, Lembo A, Fisher M, Kupersmith C, Madonick D, Moszczynski P, Smieszek S, Xiao C, Birznieks G, Polymeropoulos MH. The efficacy of tradipitant in patients with diabetic and idiopathic gastroparesis in a phase 3 randomized placebo-controlled clinical trial. Clin Gastroenterol Hepatol 2024;22:2506-2516.

66. McCallum RW, Soykan I, Sridhar KR, Ricci DA, Lange RC, Plankey MW. Delta-9-tetrahydrocannabinol delays the gastric emptying of solid food in humans: a double-blind, randomized study. Aliment Pharmacol Ther 1999;13:77-80.

67. Parkman HP, Sharkey EP, Nguyen LA, et al. Marijuana use in patients with symptoms of gastroparesis: prevalence, patient characteristics, and perceived benefit. Digest Dis Sci 2020;65:2311-2320.

68. Zheng T, BouSaba J, Taylor A, Dilmaghani S, Busciglio I, Carlson P, Torres M, Ryks M, Burton D, Harmsen WS, Camilleri M. A randomized, controlled trial of efficacy and safety of cannabidiol in idiopathic and diabetic gastroparesis. Clin Gastroenterol Hepatol 2023;21:3405-3414.e4.

69. de Almeida DL, Devi LA. Diversity of molecular targets and signaling pathways for CBD. Pharmacol Res Perspect 2020;8:e00682. 

70.  Parkman HP, Van Natta ML, Abell TL, McCallum RW, Sarosiek I, Nguyen L, Snape WJ, Koch KL, Hasler WL, Farrugia G, Lee L, Unalp-Arida A, Tonascia J, Hamilton F, Pasricha PJ. Effect of nortriptyline on symptoms of idiopathic gastroparesis: the NORIG randomized clinical trial. JAMA 2013;310:2640-2649.

71. Yang D, Abdelnaem N, Matar A, Camilleri M. Gastric accommodation and impact on emptying of solids in gastroparesis. Neurogastroenterol Motil (submitted)

72. Liau SS, Camilleri M, Kim DY, Stephens D, Burton DD, O’Connor MK. Pharmacological modulation of human gastric volumes demonstrated noninvasively using SPECT imaging. Neurogastroenterol Motil 2001;13:533-542.  

73. Coulie B, Tack J, Peeters T, Janssens J. Involvement of two different pathways in the motor effects of erythromycin on the gastric antrum in humans. Gut 1998;43:395-400.

74. Richards RD, Davenport K, McCallum RW. The treatment of idiopathic and diabetic gastroparesis with acute intravenous and chronic oral erythromycin. Am J Gastroenterol 1993;88:203-207.

75. Park S-Y, Acosta A, Camilleri M, Fox J, Szarka LA. Gastric motor dysfunction in patients with functional gastroduodenal symptoms. Am J Gastroenterol 2017;112:1689-1699.

76. Chial HJ, Camilleri M, Burton D, Thomforde G, Olden KW, Stephens D. Selective effects of serotonergic psychoactive agents on gastrointestinal functions in health. Am J Physiol Gastrointest Liver Physiol 2003;284: G130-G137.

77. Parkman HP, Yates KP, Sarosiek I, Bulat RS, Abell TL, Koch KL, Kuo B, Grover M, Farrugia G, Silver P, Abdullah A, Maurer AH, Malik Z, Miriel LA, Tonascia J, Hamilton F, Pasricha PJ, McCallum RW; NIDDK Gastroparesis Clinical Research Consortium. Buspirone for early satiety and symptoms of gastroparesis: A multi-centre, randomised, placebo-controlled, double-masked trial (BESST). Aliment Pharmacol Ther 2023;57:1272-1289.

78. Carbone F, Vanuytsel T, Tack J. The effect of mirtazapine on gastric accommodation, gastric sensitivity to distention, and nutrient tolerance in healthy subjects. Neurogastroenterol Motil 2017 Dec;29(12). doi: 10.1111/nmo.13146. Epub 2017 Jul 11.  

79. Thomas A, de Souza Ribeiro B, Malespin M, de Melo SW Jr. Botulinum toxin as a treatment for refractory gastroparesis: a literature review. Curr Treat Options Gastroenterol 2018;16:479-488.

80. Friedenberg FK, Palit A, Parkman HP, Hanlon A, Nelson DB. Botulinum toxin A for the treatment of delayed gastric emptying. Am J Gastroenterol 2008;103:416-423. 

81. Arts J, Holvoet L, Caenepeel P, Bisschops R, Sifrim D, Verbeke K, Janssens J, Tack J. Clinical trial: a randomized-controlled crossover study of intrapyloric injection of botulinum toxin in gastroparesis. Aliment Pharmacol Ther 2007;26:1251-1258.

82. Vosoughi K, Ichkhanian Y, Jacques J, et al. Role of endoscopic functional luminal imaging probe in predicting the outcome of gastric peroral endoscopic pyloromyotomy. Gastrointest Endosc 2020;91:1289-1299.

83. Desprez C, Melchior C, Wuestenberghs F, et al. Pyloric distensibility measurement predicts symptomatic response to intrapyloric botulinum toxin injection. Gastrointest Endosc 2019;90:754-760.e1.  

84. Martinek J, Hustak R, Mares J, Vackova Z, Spicak J, Kieslichova E, Buncova M, Pohl D, Amin S, Tack J. Endoscopic pyloromyotomy for the treatment of severe and refractory gastroparesis: a pilot, randomised, sham-controlled trial. Gut 2022;71:2170-2178.

85. Shada AL, Dunst CM, Pescarus R, et al. Laparoscopic pyloroplasty is a safe and effective first-line surgical therapy for refractory gastroparesis. Surg Endosc 2016;30:1326-1332.

Download Tables, Images & References

Dispatches from the GUILD Conference 2025

Introduction: Dispatches from the GUILD Conference 2025

March 2025 • Volume XLIX, Issue 3
Uma Mahadevan

Read Article

Welcome to the ninth annual Dispatches from the GUILD Conference series. The Gastrointestinal Updates-IBD-Liver Disease (GUILD) Conference is an annual CME conference held in Maui, Hawaii every February (GUILD 2025: February 16 -19) and a new meeting in the Caribbean, this year in St. Thomas, in January 2025. We are delighted to offer a hybrid meeting with over 250 health care providers attending live. GUILD again provides cutting edge updates in gastroenterology by world class speakers. Our topics this year include 2 days of IBD updates, a day of hepatology and a day devoted to general gastroenterology including eosinophilic esophagitis, gastroparesis and obesity. We understand that trainees are our future. Ten Gastroenterology fellows were selected to attend the meeting and receive daily mentoring and networking from our star faculty. GUILD also recognizes the role played by nurse practitioners and physician assistants in the care of IBD and liver patients and introduced a boot camp in 2019, awarding 10 scholarships to APPs to attend the meeting.

To share our learning with the gastroenterology community at large, we are happy to continue our series beginning with the following article,
“Diagnosis and Management of Gastroparesis”.

We look forward to providing informative and educational articles covering IBD, Hepatology, and key topics in general gastroenterology in Practical Gastroenterology over the following months. We hope to see you all in person for GUILD 2026 in Puerto Rico (January 11-14, 2026) and in Maui (February 14 -18, 2026). 

For more information on the
GUILD Conference, visit:

guildconference. com

Download Tables, Images & References

Frontiers in Endoscopy, Series #94

Endoscopic Management of Esophageal and Gastric Anastomotic Strictures

March 2025 • Volume XLIX, Issue 3
Michael B. Andrews,Douglas G. Adler

Read Article

Introduction

Esophageal and gastric anastomotic strictures can be challenging to treat. Minimally-invasive therapeutic endoscopic intervention has overtaken surgical re-intervention as first-line therapy. This literature review aims to assess the technique, efficacy, and adverse events of the many currently available options for endoscopic management.

Esophageal Anastomotic Strictures

Etiology

Esophageal anastomotic strictures (EAS) are most commonly a post-operative adverse event following esophagectomy and esophageal atresia repair. The most common indication for esophagectomy is treatment of malignancy, but rarely, it may be indicated for treatment of benign esophageal disease in cases of severe obstruction, perforation, or dysmotility. EAS remains a common problem. The reported rate of EAS following esophagectomy ranges between 5-46% with a large retrospective cohort study performed by Honkoop et al. demonstrating EAS development in 114 out of 269 (42%) patients.2,3

Esophageal atresia is a rare congenital anomaly affecting 1 in 3,500 births.4 There are four types (A-D) of esophageal atresia of which type C is seen in 80-85% of cases and presents anatomically with a closed off upper esophagus and aberrant connection of the lower esophagus to the trachea.5,6 Surgical repair is required, but post-operative EAS has been reported to develop in approximately one-third to one-half of patients.4,7,8

Risk Factors

Patient risk factors for EAS include pre-operative cardiovascular disease and diabetes.2,9 Mendelson et al. reported lower risk for EAS in patients who had previously received neoadjuvant chemotherapy when esophagectomy was performed for malignancy.

Surgical risk factors have been more extensively studied with data supporting post-operative anastomotic leakage as a driver of tissue ischemia, inflammation and eventual stricture development.2,9 Anastomotic closure techniques, hand-sewn versus stapled, have also been analyzed without clear evidence to suggest one increases risk for EAS more than the other.11,12

Clinical Manifestations

Dysphagia is the most common clinical manifestation of EAS, described by patients as the inability to swallow, food becoming stuck in the throat, or regurgitation of food.13 Dysphagia can be graded using the Atkinson’s classification: grade 0 (ability to tolerate normal diet), grade 1 (ability to swallow some solids), grade 2 (ability to swallow semi-solids), grade 3 (ability to swallow liquids), and grade 4 (inability to swallow anything).14

Bougie and Endoscopic Balloon Dilation

Technique – Bougie Dilation

Bougie dilators are reusable push-type dilators available in various sizes with a fixed diameter exerting radial and longitudinal forces simultaneously as they pass through the stricture.15 Hurst and Maloney bougie dilators (Medovations, Milwaukee, Wisc, and Teleflex Medical, Research Triangle Park, NC) do not use a guidewire and are instead pushed blindly with gravity assistance from tungsten within the dilator.15 Savary-Gillard (Cook Medical, Winston-Salem, NC) and American Dilation System bougie dilators (ConMed, Utica, NY) utilize a guidewire placed endoscopically followed by passage of the bougie dilator over the wire, with or without fluoroscopic guidance.15 Available diameters range from 16-60 French (Hurst), 36-54 French (Maloney), and 15-60 French (Savary-Gillard and American Dilation System).15

Technique – Endoscopic Balloon Dilation

Balloon dilators are single-use, inflatable dilators of various diameters (6-20mm) designed to supply a radial force against the stricture.15 The most common technique utilizes a through-the-scope (TTS) balloon dilator passed over a guidewire to position the balloon within the stricture prior to inflation with injection of saline or contrast.15 Others are designed to be placed through the scope under endoscopic visualization without a guidewire, but these are rarely used in modern clinical practice.15

Efficacy

Results across multiple studies are similar for both bougie and endoscopic balloon dilation (EBD) with initial clinical success rates ranging from 70-90% following a median of two to nine dilation sessions, emphasizing how refractory some of these strictures can be.2,14,16,17  van Halsema et al., in a retrospective cohort study of 179 patients, reported a stricture recurrence rate of 73.7%.18 Risk factors for recurrence include diabetes and strictures longer than 10mm.17 van Halsema et al. also showed significantly increased dilation-free days (92 vs. 41 days) and decreased recurrence rates (68.1% vs. 79.5%) with dilation >16mm diameter compared to 16mm.18 There were no significant differences in adverse events including perforation between the two groups.18

Adverse Events

van Halsema et al. reported an overall adverse event rate of 5.3% per patient and 1.0% per procedure.18 The most notable adverse events were perforation rates of 3.6% per patient and 0.6% per procedure with bleeding in <1% of patients.18

Adjunctive Triamcinolone Injection

Technique

Intralesional injection of triamcinolone acetonide has been studied in multiple randomized control trials as adjunctive therapy to dilation of EAS.19,20  Local steroid injection is thought to inhibit fibrotic healing and scar contracture following dilation.21 While widely employed, steroid dosages and injection techniques vary based on operator preference and institutional experience. A meta-analysis by Dasari et al. reported dosages ranging from 40-50mg with multiple intralesional injections using a 25-gauge needle.19,22

Efficacy

Hanaoka et al. performed a randomized control trial of 65 patients and observed a two-fold reduction in the median number of dilation sessions required to achieve clinical success with adjunctive steroid injection compared to dilation alone.19 The patients in the treatment arm also had a significantly higher six-month recurrence-free rate of 39% compared to 16% in the control arm (p-value < 0.01).19 Pereira-Lima et al., in a randomized control trial limited by a small sample size of only 19 patients, had previously reported similar findings with a significantly higher six-month recurrence-free rate of 62% in the treatment arm compared to 0% in the control arm (p-value <0.01).20

Adverse Events

Neither Hanaoka et al. nor Pereira-Lima et al. reported any adverse events in their 84 combined patients including bleeding, pain, perforation, or Candida esophagitis.19,20 However, in a more recent meta-analysis published in 2020, Dasari et al. reported a perforation rate of 1.4% and a Candida esophagitis rate of 5.5%.22 

Self-Expandable Metal Stents

Technique

The first endoscopic stent type used to treat EAS was a self-expandable plastic stent (SEPS).23 SEPS required assembly, were cumbersome to place, had high migration rates, and, despite some good clinical outcomes, are essentially obsolete and have since been replaced by self-expandable metal stents (SEMS).23,24 

Modern SEMS have strong radial force and are available as uncovered (UCSEMS), partially covered (PCSEMS), or fully covered (FCSEMS) devices. Commercially available stents in the United States include WallFlex stents (Boston Scientific, Natick, Massachusetts, United States), Endomaxx and Alimaxx stents (Merit Medical, South Jordan, Utah, United States), and Evolution stents (Cook Endoscopy, Winston-Salem, North Carolina, United States).25,26 These stents are available in various lengths (6-16cm) and diameters (12-23mm) and are designed to prevent migration via proximal and/or distal flared ends with various stent designs including fins and scaling to further reduce migation.25 Stents can be placed via endoscopy, fluoroscopy, or a combination thereof. (Figure 1)

Efficacy

Four retrospective cohort studies have shown clinical success rates ranging from 21-70%, but no individual study contained more than 50 patients with EAS.27,28,29,30  Wu et al. treated EAS with PCSEMS showing a 12-month stricture-free recurrence rate of 70% and a mean improvement of one point in dysphagia grade.27 Re-stenting was required in 12 out of 13 patients treated in the retrospective study performed by Suzuki et al. using various types of SEMS, reflecting that many of these strictures can be refractory.28 Bakken et al. and Eloubeidi et al. reported use of FCSEMS with stricture recurrence rates at approximately two months of 30% and 79%, respectively.29,30

Adverse Events

Stent migration remains a common adverse event occurring in approximately one-third of patients.31  Suzuki et al. reported a similar migration rate of 38.5% in EAS patients using various types of SEMS.28 The two studies that used only FCSEMS reported migration rates of 37.3% and 60%.29,30 No perforations were reported among the four studies, but there was one incident of food impaction within the stent at day 128.27,28,29,30

It should be stressed that sometimes migration is not a true adverse event and may reflect the fact that the stricture has resolved, thus allowing the stent to migrate. This concept was highlighted by Thomas et al. in a large retrospective cohort study of 369 patients with benign or malignant esophageal strictures treated with various FCSEMS.32 They observed total migration rates of 23-30% with clinically relevant migration rates of only 14-17%.32

Migration rates can be reduced using different anchoring techniques.31 These include endoscopic suturing (which is more technically challenging and expensive) with a reported 17% migration rate.33  Other techniques include deploying TTS or over-the-scope (OTS) clips with lower reported migration rates of 13% and 6.7-15%, respectively.31,34 An FDA-approved stent fixation device on the market since 2019, the Stentfix OTS Clip System (Ovesco, AG-Tuebingen Germany), was prospectively studied by Manta et al. who reported a migration rate of only 3.2% and no adverse events when used.31

Lumen-Apposing Metal Stents

Technique

Lumen-apposing metal stents (LAMS) were originally approved by the FDA to drain pancreatic fluid collections but have since been widely used for the endoscopic treatment of a variety of other conditions, including EAS, in an off-label manner. LAMS are fully covered, short stents with wide proximal and distal flanges to reduce migration.35 The only commercially available LAMS in the United States is the AXIOS stent (Boston Scientific, Natick MA, United States) with a 10mm length, 6-15mm diameter, and flanges of 21 or 24mm diameter.35,37 A guidewire is placed across the stricture under endoscopic and fluoroscopic guidance, and the stent is deployed with or without pre-stent or in-stent dilation.35,37 (Figure 2) Stent dwell time has been commonly reported between 60-90 days, but is often individualized.38,39 

Efficacy

LAMS have been used for short (<1cm) EAS with reported clinical success rates ranging from 50-100% among two case series and two retrospective cohort studies that combined reported on 17 patients.36,37,38,39 The largest of these, an international multicenter retrospective cohort study by Santos-Fernandez, included seven patients with EAS and showed a 30-day symptom resolution rate of >80% which dropped to <50% at 90 days.36 Larger studies specifically focused on use in EAS patients are needed.

Adverse Events

Out of the 17 patients, there were three (17.6%) stent migrations, two (11.8%) angulations, and development of a new proximal stricture made of granulation tissue in one case requiring balloon dilation to remove the stent.36,37,38,39 No study reported bleeding or perforation.36,37,38,39

Biodegradable Stents

Technique

Biodegradable stents (BDS) made of synthetic polymers such as polydioxanone are designed to apply a radial force for approximately six weeks then degrade via hydrolysis over an additional six to 24 weeks.40 This eliminates the need for a removal procedure, but the currently available BDS require assembly and supply a weaker radial force than traditional SEMS.40 The SX-ELLA BDS (ELLA-CS, Hradec Kralove, Czech Republic) is the only commercially available BDS for esophageal use and is available in many lengths (60-135mm) and diameters (18-25mm).41 This device is not approved for use in the United States. Once assembled, BDS are loaded onto a delivery system, advanced over a guidewire, and deployed with endoscopic and/or fluoroscopic visualization using radiopaque markers on both ends.41

Efficacy

There are limited studies on BDS for treatment of EAS. Sanchez Munoz et al.’s case report described an ideal sequence of events with successful placement, initial stent degradation at four weeks, complete stent resorption at five months, and a patent anastomosis without symptoms at 20-month follow-up.42 Three prospective cohort studies with a combined 21 EAS patients reported clinical success rates of 25-60% with median dysphagia-free time of three to six months.43,44,45  However, several patients experienced stricture recurrence requiring up to three BDS replacements to maintain long-term patency.43,44,45

Adverse Events

Using BDS, Hirdes et al. reported bleeding, stent migration, and food impaction in 11% and pain in 7% of patients.43 van Boeckel et al. reported bleeding, pain, food impaction, and tissue overgrowth in 11% and stent migration in 22% of patients.44 van Hooft et al. reported food impaction in 10% and obstruction due to stent epithelialization in 20% of patients.45 Perforation was not reported in any of the studies.43,44,45

Endoscopic Incisional Therapy

Technique

Endoscopic incisional therapy (EIT) was first used to treat Schatzki rings and has been applied to refractory benign esophageal strictures as well.46  Radial incision and cutting (RIC) is one method using an insulation-tip (IT) knife (KD611L, IT2, Olympus, Japan) or a standard needle knife to make radial incisions around the circumference of the stricture, sometimes with removal of the fibrotic tissue in-between incisions.47,48,49,50  Radial incisions of operator-dependent length and depth are made perpendicular to the stricture.49,50

Efficacy

Clinical success of EIT ranges from 50-100% across multiple studies.46,47,48,49,50 Two retrospective cohort studies with a combined 104 patients showed 50-63% of patients remained asymptomatic at six months.46,47 In a case series of 20 patients, Hordijk et al. observed the 12 patients with strictures <1cm long remained asymptomatic at 12 months whereas 8 patients with strictures >1cm long experienced dysphagia recurrence.49

Jimoh et al. performed a meta-analysis showing EIT significantly reduced the odds (OR 0.32, p-value 0.03) of stricture recurrence in naïve EAS compared to EBD.51 Muto et al.’s retrospective cohort study showed similar results with significantly higher 6-month (65.3% vs. 19.8%, p-value <0.005) and 12-month (61.5% and 19.8%, p-value <0.005) recurrence-free rates in patients treated with EIT compared to EBD.47

Adverse Events

Chest pain (up to 26%) was a commonly reported adverse event among published studies.46,48 Bleeding was reported in 10% of patients.46 There were no reports of perforation.46,48,49,50

Gastric Anastomotic Strictures

Etiology

Gastric anastomotic strictures most commonly develop following Roux-en-Y gastric bypass (RYGB) surgery but may also result following gastric resections for benign or malignant disease.52,53  Gastric anastomotic strictures account for half of RYGB post-operative adverse events affecting 3-28% of patients.52,53

Risk Factors

Patient risk factors for gastric anastomotic strictures include pre-operative gastroesophageal reflux disease. Risk for concomitant marginal ulcers increased in patients using tobacco, alcohol, or non-steroidal anti-inflammatory drugs (NSAIDS).55

Many studies have examined the impact of anastomotic closure techniques on the risk for developing gastric anastomotic strictures with conflicting results.52,, Jiang et al. performed a meta-analysis of 13,626 patients showing no significant difference in gastric anastomotic stricture rates between hand-sewn, circularly stapled, or linearly stapled anastomoses following laparoscopic RYGB.56 However, a more recent meta-analysis by Jin et al. reported patients were at higher risk for gastric anastomotic strictures if circular stapling was used compared to linear stapling.57

Clinical Manifestations

Patients often present with obstructive symptoms including nausea, vomiting, early satiety, reflux, and/or dysphagia.52, Carrodeguas et al. performed a retrospective cohort study of 1,291 patients noting mean symptom onset at 52 days (range 20-154 days) following surgery.58 

Endoscopic Balloon Dilation

Technique

TTS EBD is the most utilized method for dilating gastric anastomotic strictures. Clinicians target a RYGB stoma diameter of 10-12mm.52 The same EBD techniques described previously apply to gastric anastomotic stricture dilation with the balloon dilator positioned with or without a guidewire prior to inflation against the stricture.15

Efficacy

Meta-analyses by Baumann et al. (N=896) and Campos et al. (N=760) showed clinical success rates of 97% and 98%, respectively.53,59 Baumann et al. noted only 38% of patients required multiple dilation sessions, and Campos et al. reported patients required a mean of 1.62 dilation sessions to achieve clinical success.53,59

Adverse Events

Perforation occurred in 1.8-2.3% of patients.53,59 Baumann et al. reported only one incidence of bleeding out of 896 patients.59

Self-Expandable Metal Stents

Technique

The main barrier to using SEMS to treat gastric anastomotic strictures is the ability to reach the stricture with the stent delivery system. Many of the previously described esophageal SEMS, especially the Endomaxx stents (Merit Medical, South Jordan, Utah, United States), can be used off-label if the stricture is within reach of the stent’s sheath.25 Cai et al. described successful use of longer FCSEMS Megastents (Taewoong Medical Industries, Kangseo-Gu Songjung-Dong, South Korea) available as 18 and 23cm to reach distal strictures.52 This stent is designed with flares to reduce migration rates.52 The Wallstent Enteral and Wallflex Duodenal stents (Boston Scientific, Natick, Massachusetts, United States) are other options available in lengths 60-120cm and diameters 20-22mm.25

Efficacy

Limited data exist regarding treatment of gastric anastomotic strictures with SEMS.60,61,62  Randhawa et al. performed a prospective cohort study with six gastric anastomotic stricture patients showing an 83.3% clinical success rate.61 Bakken et al.’s retrospective cohort study with 12 gastric anastomotic stricture patients described a clinical success rate of 75% at the time of stent removal but a 77% recurrence rate.62

Adverse Events

Stent migration is a commonly experienced adverse event seen in up to 50% of patients.61,62 Previously described SEMS anchoring techniques may be used to reduce stent migration.61 Randhawa et al. observed a decrease in migration rate from 28.6% to 0% when more than one endoscopic suture was applied to the FCSEMS.61 Only one perforation was reported out of 19 patients.60,61,62

Lumen-Apposing Metal Stents

Technique

LAMS can be used in an off-label manner to treat gastric anastomotic strictures using the same technique described above for EAS.63  (Figure 3) While operator dependent, Skidmore et al. described a case series of 14 patients where pre-stent dilation was avoided with the goal of reducing stent migration.

Efficacy

Clinical success using LAMS ranges from 60-100% across many studies including a retrospective cohort study of 109 patients performed by Mahmoud et al. who reported 98.4% of patients were asymptomatic at 30 days.63,64,65,66,67,68  However, stricture recurrence requiring re-intervention occurred in approximately half of patients.68

Adverse Events

Stent migration occurred in 10-27.3% of patients.64,67,68 Chest pain was experienced by as many as 10-14% of patients.64,68 Mahmoud et al. reported bleeding in 3.9% of patients.68 Only one perforation was reported out of 154 total patients across all studies.64,65,66,67,68

Conclusion

Treatment of esophageal and gastric anastomotic strictures remains a significant challenge despite advancement in therapeutic endoscopic options. For esophageal anastomotic strictures, bougie and endoscopic balloon dilation remain first-line therapy despite high recurrence rates which are improved with adjunctive steroid injection. Other modalities include stent placement with SEMS, LAMS, or BDS, each with varying degrees of efficacy and adverse events, as well as endoscopic incisional therapy. Endoscopic management options for gastric anastomotic strictures are similar including endoscopic balloon dilation, if technically feasible based on stricture location, and stent placement with SEMS or LAMS. 

References

1. Mormando J, Barbetta A, Molena D. Esophagectomy for benign
disease. J Thorac Dis. 2018;10(3):2026-2033. doi:10.21037/
jtd.2018.01.165
2. Honkoop P, Siersema PD, Tilanus HW, Stassen LP, Hop WC, van
Blankenstein M. Benign anastomotic strictures after transhiatal esophagectomy
and cervical esophagogastrostomy: risk factors and
management. J Thorac Cardiovasc Surg. 1996;111(6):1141-1148.
doi:10.1016/s0022-5223(96)70215-5
3. Gu YM, Yang YS, Shang QX, Wang WP, Yuan Y, Chen LQ. Risk factors
for benign anastomotic stricture post-oesophagectomy: single-centre
analysis of 702 oesophagectomies with squamous cell carcinoma.
Transl Cancer Res. 2019;8(3):828-835. doi:10.21037/tcr.2019.05.06
4. Baghdadi O, Yasuda J, Staffa S, et al. Predictors and Outcomes of
Fully Covered Stent Treatment for Anastomotic Esophageal Strictures
in Esophageal Atresia. J Pediatr Gastroenterol Nutr. 2022;74(2):221-
226. doi:10.1097/MPG.0000000000003330
5. Evanovich DM, Wang JT, Zendejas B, Jennings RW, Bajic D.
From the Ground Up: Esophageal Atresia Types, Disease Severity
Stratification and Survival Rates at a Single Institution. Front Surg.
2022;9:799052. Published 2022 Mar 9. doi:10.3389/fsurg.2022.799052
6. Lal DR, Gadepalli SK, Downard CD, et al. Perioperative management
and outcomes of esophageal atresia and tracheoesophageal
fistula. J Pediatr Surg. 2017;52(8):1245-1251. doi:10.1016/j.jpedsurg.
2016.11.046
7. Baird R, Laberge JM, Lévesque D. Anastomotic stricture after esophageal
atresia repair: a critical review of recent literature. Eur J Pediatr
Surg. 2013;23(3):204-213. doi:10.1055/s-0033-1347917
8. Tambucci R, Angelino G, De Angelis P, et al. Anastomotic Strictures after Esophageal Atresia Repair: Incidence, Investigations, and
Management, Including Treatment of Refractory and Recurrent Strictures.
Front Pediatr. 2017;5:120. Published 2017 May 29. doi:10.3389/
fped.2017.00120
9. Zhong Y, Sun R, Li W, et al. Risk factors for esophageal anastomotic
stricture after esophagectomy: a meta-analysis. BMC Cancer.
2024;24(1):872. Published 2024 Jul 19. doi:10.1186/s12885-024-
12625-8
10. Mendelson AH, Small AJ, Agarwalla A, Scott FI, Kochman ML. Esophageal
anastomotic strictures: outcomes of endoscopic dilation, risk
of recurrence and refractory stenosis, and effect of foreign body removal.
Clin Gastroenterol Hepatol. 2015;13(2):263-271.e1. doi:10.1016/j.
cgh.2014.07.010
11. Deng XF, Liu QX, Zhou D, Min JX, Dai JG. Hand-sewn vs. linearly
stapled esophagogastric anastomosis for esophageal cancer: a metaanalysis.
World J Gastroenterol. 2015;21(15):4757-4764. doi:10.3748/
wjg.v21.i15.4757
12. Castro PM, Ribeiro FP, Rocha Ade F, Mazzurana M, Alvarez GA.
Hand-sewn versus stapler esophagogastric anastomosis after esophageal
ressection: systematic review and meta-analysis. Arq Bras Cir Dig.
2014;27(3):216-221. doi:10.1590/s0102-67202014000300014
13. Wu P, Wang F, Wu X, et al. Comparison of esophageal stent placement
versus endoscopic incision method for treatment of refractory
esophageal anastomotic stricture. Ann Palliat Med. 2019;8(4):462-468.
doi:10.21037/apm.2019.09.07
14. Hordijk ML, van Hooft JE, Hansen BE, Fockens P, Kuipers EJ. A
randomized comparison of electrocautery incision with Savary bougienage
for relief of anastomotic gastroesophageal strictures. Gastrointest
Endosc. 2009;70(5):849-855. doi:10.1016/j.gie.2009.02.023
15. ASGE Technology Committee, Siddiqui UD, Banerjee S, et al. Tools
for endoscopic stricture dilation. Gastrointest Endosc. 2013;78(3):391-
404. doi:10.1016/j.gie.2013.04.170
16. Hordijk ML, Siersema PD, Tilanus HW, Kuipers EJ. Electrocautery
therapy for refractory anastomotic strictures of the esophagus. Gastrointest
Endosc. 2006;63(1):157-163. doi:10.1016/j.gie.2005.06.016
17. Choi CW, Kang DH, Kim HW, et al. Clinical Outcomes of Dilation
Therapy for Anastomotic Esophageal Stricture. Korean J Gastroenterol.
2017;69(2):102-108. doi:10.4166/kjg.2017.69.2.102
18. van Halsema EE, Noordzij IC, van Berge Henegouwen MI, Fockens
P, Bergman JJ, van Hooft JE. Endoscopic dilation of benign esophageal
anastomotic strictures over 16 mm has a longer lasting effect. Surg Endosc.
2017;31(4):1871-1881. doi:10.1007/s00464-016-5187-0
19. Hanaoka N, Ishihara R, Motoori M, et al. Endoscopic Balloon Dilation
Followed By Intralesional Steroid Injection for Anastomotic Strictures
After Esophagectomy: A Randomized Controlled Trial. Am J Gastroenterol.
2018;113(10):1468-1474. doi:10.1038/s41395-018-0253-y
20. Pereira-Lima JC, Lemos Bonotto M, Hahn GD, et al. A prospective
randomized trial of intralesional triamcinolone injections after endoscopic
dilation for complex esophagogastric anastomotic strictures: steroid
injection after endoscopic dilation. Surg Endosc. 2015;29(5):1156-
1160. doi:10.1007/s00464-014-3781-6
21. Kochhar R, Poornachandra KS. Intralesional steroid injection therapy
in the management of resistant gastrointestinal strictures. World J
Gastrointest Endosc. 2010;2(2):61-68. doi:10.4253/wjge.v2.i2.61
22. Dasari CS, Jegadeesan R, Patel HK, et al. Intralesional steroids and
endoscopic dilation for anastomotic strictures after esophagectomy:
systematic review and meta-analysis. Endoscopy. 2020;52(9):721-726.
doi:10.1055/a-1172-5975
23. Evrard S, Le Moine O, Lazaraki G, Dormann A, El Nakadi I, Devière
J. Self-expanding plastic stents for benign esophageal lesions. Gastrointest
Endosc. 2004;60(6):894-900. doi:10.1016/s0016-5107(04)02278-3
24. Holm AN, de la Mora Levy JG, Gostout CJ, Topazian MD, Baron
TH. Self-expanding plastic stents in treatment of benign esophageal
conditions. Gastrointest Endosc. 2008;67(1):20-25. doi:10.1016/j.
gie.2007.04.031
25. ASGE Technology Committee, Varadarajulu S, Banerjee S, et al.
Enteral stents. Gastrointest Endosc. 2011;74(3):455-464. doi:10.1016/j.
gie.2011.04.011
26. Thomas S, Siddiqui AA, Taylor LJ, et al. Fully-covered esophageal
stent migration rates in benign and malignant disease: a multicenter
retrospective study. Endosc Int Open. 2019;7(6):E751-E756.
doi:10.1055/a-0890-3284
27. Wu P, Wang F, Wu X, et al. Comparison of esophageal stent placement
versus endoscopic incision method for treatment of refractory
esophageal anastomotic stricture. Ann Palliat Med. 2019;8(4):462-468.
doi:10.21037/apm.2019.09.07
28. Suzuki T, Siddiqui A, Taylor LJ, et al. Clinical Outcomes, Efficacy,
and Adverse Events in Patients Undergoing Esophageal Stent Placement
for Benign Indications: A Large Multicenter Study. J Clin Gastroenterol.
2016;50(5):373-378. doi:10.1097/MCG.0000000000000500
29. Bakken JC, Wong Kee Song LM, de Groen PC, Baron TH. Use
of a fully covered self-expandable metal stent for the treatment of benign
esophageal diseases. Gastrointest Endosc. 2010;72(4):712-720.
doi:10.1016/j.gie.2010.06.028
30. Eloubeidi MA, Talreja JP, Lopes TL, Al-Awabdy BS, Shami VM,
Kahaleh M. Success and complications associated with placement of
fully covered removable self-expandable metal stents for benign esophageal
diseases (with videos). Gastrointest Endosc. 2011;73(4):673-681.
doi:10.1016/j.gie.2010.11.014
31. Manta R, Del Nero L, Todd B, et al. Newly designed OTS Clip for
preventing fully-covered self-expandable metal stent migration in the
gastrointestinal tract. Endosc Int Open. 2023;11(3):E284-E287. Published
2023 Mar 24. doi:10.1055/a-2032-4147
32. Thomas S, Siddiqui AA, Taylor LJ, et al. Fully-covered esophageal
stent migration rates in benign and malignant disease: a multicenter
retrospective study. Endosc Int Open. 2019;7(6):E751-E756.
doi:10.1055/a-0890-3284
33. Law R, Prabhu A, Fujii-Lau L, Shannon C, Singh S. Stent migration
following endoscopic suture fixation of esophageal self-expandable
metal stents: a systematic review and meta-analysis. Surg Endosc.
2018;32(2):675-681. doi:10.1007/s00464-017-5720-9
34. Vanbiervliet G, Filippi J, Karimdjee BS, et al. The role of clips in
preventing migration of fully covered metallic esophageal stents: a pilot
comparative study. Surg Endosc. 2012;26(1):53-59. doi:10.1007/
s00464-011-1827-6
35. Larson B, Adler DG. Lumen-apposing metal stents for gastrointestinal
luminal strictures: current use and future directions. Ann Gastroenterol.
2019;32(2):141-146. doi:10.20524/aog.2018.0337
36. Santos-Fernandez J, Paiji C, Shakhatreh M, et al. Lumen-apposing
metal stents for benign gastrointestinal tract strictures: An international
multicenter experience. World J Gastrointest Endosc. 2017;9(12):571-
578. doi:10.4253/wjge.v9.i12.571
37. Yang D, Nieto JM, Siddiqui A, et al. Lumen-apposing covered
self-expandable metal stents for short benign gastrointestinal
strictures: a multicenter study. Endoscopy. 2017;49(4):327-333.
doi:10.1055/s-0042-122779
38. Adler DG. Lumen-Apposing Metal Stents for the Treatment
of Refractory Benign Esophageal Strictures. Am J Gastroenterol.
2017;112(3):516-517. doi:10.1038/ajg.2016.566
39. Irani S, Jalaj S, Ross A, Larsen M, Grimm IS, Baron TH. Use of a
lumen-apposing metal stent to treat GI strictures (with videos). Gastrointest
Endosc. 2017;85(6):1285-1289. doi:10.1016/j.gie.2016.08.028
40. Ferreira-Silva J, Medas R, Girotra M, Barakat M, Tabibian JH, Rodrigues-
Pinto E. Futuristic Developments and Applications in Endoluminal
Stenting. Gastroenterol Res Pract. 2022;2022:6774925. Published
2022 Jan 11. doi:10.1155/2022/6774925
41. Gkolfakis P, Siersema PD, Tziatzios G, Triantafyllou K, PapanS W A L L O W C R O H N S
T U A A Y R E E
ikolaou IS. Biodegradable esophageal stents for the treatment of refractory
benign esophageal strictures. Ann Gastroenterol. 2020;33(4):330-
337. doi:10.20524/aog.2020.0482
42. Sánchez Muñoz D, Ortiz-Moyano C, Gómez-Rodríguez B. Resolution
of a refractory anastomotic stricture with a novel biodegradable
esophageal stent. Clin Gastroenterol Hepatol. 2013;11(9):e63.
doi:10.1016/j.cgh.2012.11.023
43. Hirdes MM, Siersema PD, van Boeckel PG, Vleggaar FP. Single
and sequential biodegradable stent placement for refractory benign
esophageal strictures: a prospective follow-up study. Endoscopy.
2012;44(7):649-654. doi:10.1055/s-0032-1309818
44. van Boeckel PG, Vleggaar FP, Siersema PD. A comparison of temporary
self-expanding plastic and biodegradable stents for refractory benign
esophageal strictures. Clin Gastroenterol Hepatol. 2011;9(8):653-
659. doi:10.1016/j.cgh.2011.04.006
45. van Hooft JE, van Berge Henegouwen MI, Rauws EA, Bergman
JJ, Busch OR, Fockens P. Endoscopic treatment of benign anastomotic
esophagogastric strictures with a biodegradable stent. Gastrointest Endosc.
2011;73(5):1043-1047. doi:10.1016/j.gie.2011.01.001
46. Wu P, Wang F, Wu X, et al. Comparison of esophageal stent placement
versus endoscopic incision method for treatment of refractory
esophageal anastomotic stricture. Ann Palliat Med. 2019;8(4):462-468.
doi:10.21037/apm.2019.09.07
47. Muto M, Ezoe Y, Yano T, et al. Usefulness of endoscopic radial
incision and cutting method for refractory esophagogastric anastomotic
stricture (with video). Gastrointest Endosc. 2012;75(5):965-972.
doi:10.1016/j.gie.2012.01.012
48. Tan Y, Liu D. Endoscopic incision for the treatment of refractory esophageal
anastomotic strictures: outcomes of 13 cases with a minimum
follow-up of 12 months. Rev Esp Enferm Dig. 2016;108(4):196-200.
doi:10.17235/reed.2016.4023/2015
49. Hordijk ML, Siersema PD, Tilanus HW, Kuipers EJ. Electrocautery
therapy for refractory anastomotic strictures of the esophagus. Gastrointest
Endosc. 2006;63(1):157-163. doi:10.1016/j.gie.2005.06.016
50. Hordijk ML, van Hooft JE, Hansen BE, Fockens P, Kuipers EJ. A
randomized comparison of electrocautery incision with Savary bougienage
for relief of anastomotic gastroesophageal strictures. Gastrointest
Endosc. 2009;70(5):849-855. doi:10.1016/j.gie.2009.02.023
51. Jimoh Z, Jogiat U, Hajjar A, et al. Endoscopic incisional therapy
for benign anastomotic strictures after esophagectomy or gastrectomy:
a systematic review and meta-analysis. Surg Endosc. 2024;38(6):2995-
3003. doi:10.1007/s00464-024-10817-8
52. Cai JX, Schweitzer MA, Kumbhari V. Endoscopic Management of
Bariatric Surgery Complications. Surg Laparosc Endosc Percutan Tech.
2016;26(2):93-101. doi:10.1097/SLE.0000000000000230
53. Campos JM, Mello FS, Ferraz AA, Brito JN, Nassif PA, Galvão-
Neto Mdos P. Endoscopic dilation of gastrojejunal anastomosis after
gastric bypass. Arq Bras Cir Dig. 2012;25(4):283-289. doi:10.1590/
s0102-67202012000400014
54. Khrucharoen U, Weitzner ZN, Chen Y, Dutson EP. Incidence and
risk factors for early gastrojejunostomy anastomotic stricture requiring
endoscopic intervention following laparoscopic Roux-en-Y gastric
bypass: a MBSAQIP analysis. Surg Endosc. 2022;36(6):3833-3842.
doi:10.1007/s00464-021-08700-x
55. Fringeli Y, Worreth M, Langer I. Gastrojejunal Anastomosis Complications
and Their Management after Laparoscopic Roux-en-Y Gastric
Bypass. J Obes. 2015;2015:698425. doi:10.1155/2015/698425
56. Jiang HP, Lin LL, Jiang X, Qiao HQ. Meta-analysis of hand-sewn
versus mechanical gastrojejunal anastomosis during laparoscopic
Roux-en-Y gastric bypass for morbid obesity. Int J Surg. 2016;32:150-
157. doi:10.1016/j.ijsu.2016.04.024
57. Jin T, Liu HD, Chen ZH, Hu JK, Yang K. Linear Stapler versus
Circular Stapler for Patients Undergoing Anastomosis for Laparoscopic
Gastric Surgery: A Meta-Analysis. J Invest Surg. 2022;35(7):1434-
1444. doi:10.1080/08941939.2022.2058126
58. Carrodeguas L, Szomstein S, Zundel N, Lo Menzo E, Rosenthal R.
Gastrojejunal anastomotic strictures following laparoscopic Roux-en-Y
gastric bypass surgery: analysis of 1291 patients. Surg Obes Relat Dis.
2006;2(2):92-97. doi:10.1016/j.soard.2005.10.014
59. Baumann AJ, Mramba LK, Hawkins RB, et al. Endoscopic Dilation
of Bariatric RNY Anastomotic Strictures: a Systematic Review
and Meta-analysis. Obes Surg. 2018;28(12):4053-4063. doi:10.1007/
s11695-018-3491-6
60. Singh A, Aggarwal M, Siddiki H. Treatment of refractory benign
gastroenteral strictures with fully covered metal stents. VideoGIE.
2021;6(7):308-310. Published 2021 Apr 28. doi:10.1016/j.
vgie.2021.03.004
61. Randhawa NK, Khalyfa A, Khan M, Ahsan N, Inamullah M, Ayub
K. Safety and Efficacy of Fully Covered Self-Expandable Metal Stents
for Benign Upper Gastrointestinal Strictures Beyond the Esophagus.
Cureus. 2022;14(11):e31439. Published 2022 Nov 13. doi:10.7759/
cureus.31439
62. Bakken, Johan MD; Song, Louis Wong Kee MD; Baron, Todd MD.
Temporary Use of a Fully Covered Self-Expandable Metal Stent for
Treatment of Bariatric Surgery Complications: 1380. American Journal
of Gastroenterology 105():p S511-S512, October 2010.
63. Hakim S, Khan Z, Shrivastava A, et al. Endoscopic Gastrointestinal
Anastomosis Using Lumen-apposing Metal Stent (LAMS) for
Benign or Malignant Etiologies: A Systematic Review and Meta-
Analysis. J Clin Gastroenterol. 2021;55(7):e56-e65. doi:10.1097/
MCG.0000000000001453
64. Skidmore AP. Use of lumen-apposing metal stents (LAMS) in the
management of gastro jejunostomy stricture following Roux-en-Y Gastric
Bypass for obesity: a prospective series. BMC Surg. 2021;21(1):314.
Published 2021 Jul 17. doi:10.1186/s12893-021-01310-3
65. Amateau SK, Lim CH, McDonald NM, Arain M, Ikramuddin S,
Leslie DB. EUS-Guided Endoscopic Gastrointestinal Anastomosis with
Lumen-Apposing Metal Stent: Feasibility, Safety, and Efficacy. Obes
Surg. 2018;28(5):1445-1451. doi:10.1007/s11695-018-3171-6
66. Mansoor MS, Tejada J, Parsa NA, Yoon E, Hida S. Off label use
of lumen-apposing metal stent for persistent gastro-jejunal anastomotic
stricture. World J Gastrointest Endosc. 2018;10(6):117-120.
doi:10.4253/wjge.v10.i6.117
67. Samuels JM, Yachimski P, Gamboa A, Spann M, Ardila-Gatas J.
Use of lumen-apposing metal stents in treating gastrojejunal anastomotic
strictures in bariatric patients. Surg Endosc. 2023;37(7):5703-5707.
doi:10.1007/s00464-023-10117-7
68. Mahmoud T, Beran A, Bazerbachi F, et al. Lumen-apposing metal
stents for the treatment of benign gastrointestinal tract strictures: a single-
center experience and proposed treatment algorithm. Surg Endosc.
2023;37(3):2133-2142. doi:10.1007/s00464-022-09715-8

Download Tables, Images & References