Dispatches from the GUILD Conference, Series #73

Prevention and Management of Postoperative Crohn’s Disease

March 2026 • Volume MMXXVI, Issue 3
Benjamin Click,Miguel Regueiro

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Postoperative recurrent Crohn’s disease is common and often clinically silent at onset, requiring objective assessments for diagnosis and surveillance. Patients with a history of multiple bowel resections, penetrating disease, or who smoke cigarettes after surgery are at highest risk for disease recurrence. Antibiotics, aminosalicylates, and immunomodulators modestly reduce the risk of clinical disease recurrence. In contrast, monoclonal antibodies, specifically anti-tumor necrosis factor (TNF) medications as well as the anti-integrin agent vedolizumab, are effective at suppressing disease recurrence and may have the potential to alter the natural course of disease after surgery. In this manuscript, the management of postoperative Crohn’s disease is summarized, and a simplified approach to prevention, monitoring, and treatment is provided.

Risk and Diagnosis of Postoperative Crohn’s Disease 

Despite significant medical therapeutic advances, as many as 20-30% Crohn’s disease (CD) patients require bowel surgery, mostly commonly for stricturing or penetrating complications, e.g., fistula, intraabdominal abscess. Surgery is not curative of CD, and postoperative recurrence (POR) of CD occurs in the majority of patients. In the pre-biologic era (circa 2000), natural history studies found that 70–90% of CD patients developed endoscopic evidence of disease activity within 1 year of their surgery, and that 30–60% of postoperative CD patients became symptomatic from recurrent disease within 3–5 years of their surgery. Consequently, up to 50% of postoperative CD patients in the pre-biologic era required repeat surgery within 5 years of their first surgery. 

Postoperative CD recurrence is often clinically silent with only 1/3 of patients reporting symptoms of CD despite endoscopic disease activity in the majority postoperatively. Thus, relying on symptoms postoperatively significantly underestimates mucosal disease activity and may miss an opportunity for disease interception. Fortunately, with increased utilization of postoperative management strategies, more modern estimates suggest the risk of recurrence is diminishing.

The degree of endoscopic disease activity correlates with subsequent progression to symptomatic recurrence. Thus, ileocolonoscopy is the current gold standard for POR assessment and is recommended to be performed within 6-12 months postoperatively. More delayed endoscopic assessments are associated with worse clinical outcomes. Disease activity is traditionally estimated using the Rutgeerts score, which defines activity on a 0 (normal) to 4 (severe) scale based on the extent of aphthous ulcerations in the neoterminal ileum. The more severe the endoscopic recurrence, e.g. i3 or i4, the more likely the development of clinical symptoms, i.e. clinical recurrence, and requirement for future surgery, i.e. surgical recurrence.  

Table 1. Summary of Gastroenterological Society Definitions of High-Risk Features for Postoperative Crohn’s Disease Recurrence.

American College of Gastroenterology (ACG)American Gastroenterological Association (AGA) European Crohn’s and Colitis Organization (ECCO) British Society of Gastroenterology (BSG) 
Classified as high risk with ≥ 1:
• Active tobacco use (especially in women and heavy smokers)
• ≥2 prior surgeries
• presence of penetrating disease*		Classified as high risk with ≥ 1:
• Active tobacco use
• ≥2 prior surgeries for penetrating disease, with or without perianal disease
• Age <30 years		Classified as high risk with ≥ 1:
• Smoking
• ≥ 1 prior intestinal surgery
• Penetrating disease at index surgery
• Perianal location
• Granulomas or myenteric plexitis in
• resection specimen
• Extensive small bowel resection (>50 cm)

2023 ECCO workshop includes:
• Immune-mediated inflammatory diseases
• Extra-intestinal manifestations
• Prior colon involvement		Classified as high risk if actively smoking or with ≥ 2:
• Multiple resections
• Preoperative penetrating disease behavior Perianal disease
• Granulomas in resection specimen
• Myenteric plexitis in the proximal resection margin
• Extensive bowel disease (>50 cm)
*Penetrating disease classified as fistulas, abscesses, intestinal perforations


Though ileocolonoscopy is sensitive at detecting POR, the invasive nature of the test is associated with patient discomfort, high cost, and procedural risk. Thus, noninvasive assessments are of particular interest. Fecal calprotectin (FCP) levels, produced by gastrointestinal leukocytes and epithelial cells at sites of mucosal injury and inflammation, correlate with endoscopic recurrence while normal levels have a strong negative predictive value. Based on available data, FCP cutoffs between 100-150 ug/g have been proposed, identifying endoscopic recurrence with 70-89% sensitivity, 58-69% specificity, and negative predictive values > 90%. Consequently, the American Gastroenterological Association (AGA) now advocates for fecal calprotectin-guided surveillance strategies as a cost-effective alternative to universal endoscopic evaluation in lower-risk patients within the first year postoperatively.1 AGA guidelines recommend assessing FCP between 6 and 12 months postoperatively. Earlier assessments are being explored.  

Imaging modalities including computed tomography (CT) and magnetic resonance (MR) have both shown acceptable correlation to endoscopic disease activity, though they have disadvantages of cost, poorly tolerated oral contrast, radiation (CT), and limited availability (MR). Intestinal ultrasound (IUS) has emerged as a promising radiation-free, cost-effective point-of-care imaging modality capable of detecting POR with comparable accuracy to ileocolonoscopy in expert hands.2 Combining FCP assessments with IUS can further improve test characteristics. Consequently, postoperative monitoring algorithms are increasingly incorporating these non-invasive tools when available.  

Risk Factors for Postoperative Recurrence

Factors associated with POR include clinical, disease, surgical, histologic, microbiotic, and molecular characteristics. Active smoking after surgery doubles the risk of endoscopic, clinical, and surgical recurrence and smoking cessation can reduce recurrence rates. Younger age at disease onset and rapid progression (<10 years) to surgical resection may increase recurrence risk. A history of prior surgical resections for Crohn’s may impart the strongest risk for future POR.3,4 Penetrating disease behavior (fistula, abscess) at the time of surgery is associated with increased clinical and surgical recurrence. 

Surgical approach and anastomosis technique may influence POR. These include more extensive surgical resections of the mesentery as well as novel anastomotic orientations such as the Kono-S configuration. Such approaches are being explored in randomized trials. Furthermore, histologic findings in the resection specimen including presence of granulomas, myenteric and submucosal plexitis, and positive surgical margins may identify individuals at increased risk for POR.5,6

Table 2. Efficacy of various therapies and knowledge gaps for the prevention of postoperative Crohn’s disease recurrence.

Therapy/InterventionPostoperative Recurrence Prevention Relative Efficacy
Curcumin–
Vitamin D –
Enteral Nutrition+
Probiotics–
Nitroimidazole/Antibiotics+
Mesalamine–
Budesonide–
Thiopurines+
Anti-TNF+++
Vedolizumab++
Ustekinumab+
Anti-IL-23s?
Janus kinase inhibitors?

Microbiome, serologic, genetic, and other “-omics” signatures have been described in individuals who progress to POR, but data remains inconclusive for routine clinical care at the current time.

Risk stratification has been adopted in various gastroenterological societal guidelines (Table 1). Generally, patients at high risk for recurrence include those who are actively smoking, multiple prior surgical resections, and penetrating disease behavior, with or without perianal disease. Such risk stratification may help identify patients warranting more aggressive treatment and monitoring after surgery.

Medical Prophylaxis for Preventing Postoperative Crohn’s Disease

Conventional medical therapies including antibiotics (e.g. metronidazole), aminosalicylates, and immunomodulators modestly reduce the risk of clinical disease recurrence and may be considered particularly in resource-limited settings; however, comparative analyses suggest that more novel targeted therapies are more efficacious for this purpose (Table 2).7 

Anti-tumor necrosis factor (TNF) therapy postoperatively prevents endoscopic POR and may have the potential to change the natural course of Crohn’s disease after surgery. The seminal PREVENT trial demonstrated that infliximab when used prophylactically (within 2-4 weeks postoperatively) in individuals at high risk for recurrence significantly reduced endoscopic recurrence at week 76 compared to placebo (22.4% vs. 51.3%, P < 0.001), although not clinical recurrence (12.9% vs 20.0%, P=0.097).8 This protective effect appears to extend to other anti-TNFs as adalimumab has also been found to prevent POR in several studies.9-11

In addition to anti-TNFs, the anti-integrin molecule vedolizumab (VDZ) has been recently assessed for postoperative prevention. The REPREVIO randomized trial demonstrated that CD patients with at least one POR risk factor assigned to receive VDZ within 4 weeks of ICR had a 77.8% probability of having a significantly lower modified Rutgeerts score and lower proportion with severe endoscopic recurrence (mRS ≥i2b) than the placebo group.12 Rates of severe endoscopic recurrence were 23.3% and 62.2% for the VDZ and placebo groups respectively. Notably, 62.8% and 62.2% of the VDZ group and placebo group respectively were anti-TNF experienced. These findings suggest that VDZ can be an efficacious preventative strategy either in those who are anti-TNF experienced or as an initial postoperative therapy. No prospective studies have evaluated comparative efficacy between anti-TNFs and VDZ.  

Data is emerging on the effectiveness and comparative efficacy of newer biologics or oral small molecules. These include the anti-interleukin 12/23 agent ustekinumab, anti-interleukin 23 molecules, and Janus kinase inhibitors. While these molecules are often utilized clinically for the purpose of preventing recurrence, data supporting efficacy in the postoperative setting is currently lacking.

Watch and Wait: Endoscopically-Guided Postoperative Management

Given that most, but not all, patients will develop postoperative recurrent disease suggests that universal prophylactic biologic therapy in all postoperative Crohn’s disease patients would mean overtreating a subset with consequent risks and costs. An alternative strategy would be to objectively monitor individuals postoperatively and if disease activity is identified and confirmed endoscopically, then to initiative or adjust treatment at that time. Such endoscopically-guided detection and treatment of POR was assessed in the pivotal POCER study.13 The authors demonstrated that colonoscopy at 6 months after surgery with treatment escalation for identified recurrence improved endoscopic rates at 18 months compared to routine care without a 6 month colonoscopy (49% vs. 67%, P = 0.03). Furthermore, a multicenter, retrospective cohort study comparing medical prophylaxis vs. endoscopically-guided strategies found that while there was a significant reduction in 12-month  endoscopic POR in high-risk patients on medical prophylaxis when compared to the endoscopy-driven group (24.3% vs 44.5%, p=0.03), there was no significant difference in time to clinical POR for both low- and high-risk groups over the 3 year study follow up period.14 However, other retrospective studies have suggested that medical prophylaxis was associated with a significantly lower risk of endoscopic POR.15 

Strategies for Postoperative Crohn’s Disease Management

Consequently, key questions that remain in the practical management of postoperative Crohn’s disease are: (1) which patients should receive immediate postoperative therapy as prophylaxis against POR, and (2) which patients would it be reasonable to wait to treat endoscopic recurrence? Until evidence more clearly determines the optimal strategy for individual patients, the current prevailing approach for postoperative Crohn’s disease management is to stratify postoperative treatment based on risk and treat those patients at high risk for recurrence with prophylactic medical therapy (Figure 1). High risk factors include active smoking, multiple prior Crohn’s-related surgeries, penetrating disease behavior (e.g., intraabdominal fistula or abscess). The authors also consider those with residual disease (gross or positive margins) after surgery to be at high risk for POR. High-risk individuals should be considered for initiation of prophylactic biologic therapy within 4 weeks of surgery. Such risk-stratified utilization of medical prophylaxis has been shown to reduce rates; however, it should be noted that when utilized in low-risk patients, prophylaxis was similarly effective.14,16

For individuals at high risk on medical prophylaxis, or with surgical or histopathologic factors for recurrence, e.g., myenteric plexitis, transmural lesions, granulomas all requiring validation studies, one can consider incorporating early biomarker monitoring with FCP as well as IUS at 3 months postop. If FCP is elevated > 150 ug/ml or IUS features of disease activity, earlier colonoscopy (prior to month 6) to assess disease activity and adjust treatment regimen is reasonable. If these early assessments are normal or minimal, a gold standard colonoscopy between 6-12 months should be used to guide therapy and follow up decisions.  Concurrent FCP assessment (measured prior to colonoscopy preparation) is helpful if future biomarker monitoring is desired to align FCP levels to contemporaneous endoscopy findings.  

In high-risk patients who are receiving preoperative biologic therapy and plan to utilize biologic therapy postoperatively, it is important to distinguish preoperative therapeutic failure (e.g., active disease progression despite adequate drug exposure) from “failure” due to preexisting damage (e.g., fibrostenotic stricture) or complication (e.g., penetrating disease). With verified therapeutic failure, the biologic mechanism of action should be changed postoperatively. It is the authors opinion that with a preexisting stricture or complication, the preoperative biologic exposure does not necessarily represent a true therapeutic failure but was rather instituted too late in the disease course to reverse the existing tissue damage. Consequently, the agent or therapeutic class may be continued postoperatively for prophylaxis, particularly for anti-TNFs (+/- immunomodulator). Despite historical concerns about risk of perioperative complications with biologics, more recent large prospective studies controlling for confounding factors (e.g., malnutrition, steroids) have not seen a detrimental effect of perioperative biologic exposure.17 Thus, in this situation, the authors also frequently continue the biologic dosing throughout the perioperative period after discussing with the surgical team.

Low-risk patients are identified by those without prior surgical history, nonsmokers, and lacking other high-risk factors. Individuals identified as low risk for POR could refrain from prophylactic biologic therapy and instead be monitored with FCP and IUS at 3 months with subsequent colonoscopy within 12 months of surgery with treatment decisions guided by endoscopic findings.

Importantly, early endoscopic remission does not guarantee subsequent remission. Up to 50% of individuals with endoscopic remission on their index postoperative colonoscopy can experience disease progression regardless of medical therapy utilization with median time to progression of 18 months.18 Thus, those without endoscopic recurrence could be monitored with serial FCP every 3-6 months, periodic IUS, and ongoing colonoscopy surveillance in 1-2 years with subsequent intervals determined by findings. 

Figure 1. Proposed simplified algorithm for the management of postoperative Crohn’s disease stratified by postoperative recurrence risk. 

Symptoms that mimic active Crohn’s disease can occur following an ileocecal resection and it is important for providers to understand possible etiologies and diagnostic plans. Postsurgical abdominal pain or discomfort is common in the days to weeks following the event, but typically steadily dissipates with time. Non-Crohn’s potential pain etiologies to be considered include postoperative complications (anastomotic leak, abscess, hematoma), impaired gastrointestinal motility (e.g. ileus, opioid-induced constipation or gastroparesis), adhesive disease, cholelithiasis, cholecystitis, nephrolithiasis, or urinary tract infections. Increased frequency and loose consistency of bowel movements can be normal gastrointestinal consequences of a resection surgery and intestinal adaption can occur in the months following. Fiber supplementation can often improve this clinical situation. Other postoperative diarrheal states should also be considered including Clostridium difficile infection, bile acid diarrhea secondary to ileal resection, and small intestinal bacterial overgrowth. Stool pathogen panels, glucose or lactulose breath testing, and a trial of bile acid sequestrant (e.g., cholestyramine, colestipol) can be considered. Finally, individuals with extensive or multiple prior resections may be at risk of short gut syndrome with consequent malabsorptive diarrhea, dehydration, weight loss, and electrolyte disturbances.  

Postoperative health maintenance should include periodic assessments of nutritional status including Vitamin B12 and Vitamin D, immunization considerations for those on advanced therapy, monitoring weight and dietary intake, smoking cessation when applicable, and ensuring execution of the postoperative Crohn’s disease management and monitoring plan.

Conclusions

Despite medical and management advances, a significant portion of CD patients require resective surgery. Postoperative recurrence of CD is common, often silent, and requires appropriate therapeutic and monitoring strategies to prevent disease progression. Preoperative risk stratification can help identify patients who may benefit most from prophylactic medical therapy postoperatively. To date, anti-TNFs remain the most effective and studied therapy for prevention of Crohn’s disease in high-risk patients, however, vedolizumab is emerging as an option. Ongoing surveillance with fecal calprotectin and IUS, when available, and colonoscopy at 6-12 months postoperatively allows for early recurrence identification and treatment. There remain many key knowledge gaps in risk factors, biomarkers, and management algorithms for postoperative Crohn’s disease. 

Financial Disclosures

Dr. Click – Consulting for AbbVie 

Dr. Regueiro – Advisory Boards and Consultant (both) for Abbvie, Johnson and Johnson, UCB, Takeda, Pfizer, BMS, Organon, Amgen, Genentech, Gilead, Salix, Prometheus, Lilly, Celgene, Boehringer Ingelheim Pharmaceuticals Inc. (BIPI), Celltrion, Roche, Merck, Sanofi, Biocon, Abavax


References

References

1. Ananthakrishnan AN, Adler J, Chachu KA, et al. AGA Clinical Practice Guideline on the Role of Biomarkers for the Management of Crohn’s Disease. Gastroenterology. Dec 2023;165(6):1367–1399. doi:10.1053/j.gastro.2023.09.029

2. Bohra A, Van Langenberg DR, Vasudevan A. Intestinal Ultrasound in the Assessment of Luminal Crohn’s Disease. Gastrointestinal Disorders. 2022;4(4):249–262. 

3. De Cruz P, Kamm MA, Prideaux L, Allen PB, Desmond PV. Postoperative recurrent luminal Crohn’s disease: a systematic review. Inflamm Bowel Dis. Apr 2012;18(4):758-77. doi:10.1002/ibd.21825

4. Shah RS, Nakamura T, Bachour S, et al. S0825 rior Surgical History Is the Strongest Risk Factor for Postoperative Crohn’s Disease Recurrence: A Guideline-Based Risk-Stratified Analysis. Official journal of the American College of Gastroenterology | ACG. 2020;115:S424. doi:10.14309/01.ajg.0000705348.73867.ec

5. Simillis C, Jacovides M, Reese GE, Yamamoto T, Tekkis PP. Meta-analysis of the role of granulomas in the recurrence of Crohn disease. Dis Colon Rectum. Feb 2010;53(2):177-85. doi:10.1007/DCR.0b013e3181b7bfb0

6. Li Y, Stocchi L, Rui Y, Remzi FH, Shen B. Comparable outcomes of the consistent use versus switched use of anti- tumor necrosis factor agents in postoperative recurrent Crohn’s disease following ileocolonic resection. Int J Colorectal Dis. Nov 2016;31(11):1751-1758. doi:10.1007/s00384-016-2632-4

7. Singh S, Garg SK, Pardi DS, Wang Z, Murad MH, Loftus EV, Jr. Comparative efficacy of pharmacologic interventions in preventing relapse of Crohn’s disease after surgery: a systematic review and network meta-analysis. Gastroenterology. Jan 2015;148(1):64–76 e2; quiz e14. doi:10.1053/j.gastro.2014.09.031

8. Regueiro M, Feagan BG, Zou B, et al. Infliximab Reduces Endoscopic, but Not Clinical, Recurrence of Crohn’s Disease After Ileocolonic Resection. Gastroenterology. Jun 2016;150(7):1568-1578. doi:10.1053/j.gastro.2016.02.072

9. Papamichael K, Archavlis E, Lariou C, Mantzaris GJ. Adalimumab for the prevention and/or treatment of post-operative recurrence of Crohn’s disease: a prospective, two-year, single center, pilot study. J Crohns Colitis. Oct 2012;6(9):924-31. doi:10.1016/j.crohns.2012.02.012

10. Savarino E, Bodini G, Dulbecco P, et al. Adalimumab is more effective than azathioprine and mesalamine at preventing postoperative recurrence of Crohn’s disease: a randomized controlled trial. Am J Gastroenterol. Nov 2013;108(11):1731-42. doi:10.1038/ajg.2013.287

11. Savarino E, Dulbecco P, Bodini G, Assandri L, Savarino V. Prevention of postoperative recurrence of Crohn’s disease by Adalimumab: a case series. Eur J Gastroenterol Hepatol. Apr 2012;24(4):468-70. doi:10.1097/MEG.0b013e3283500849

12. D’Haens G, Taxonera C, Lopez-Sanroman A, et al. Vedolizumab to prevent postoperative recurrence of Crohn’s disease (REPREVIO): a multicentre, double-blind, randomised, placebo-controlled trial. Lancet Gastroenterol Hepatol. Jan 2025;10(1):26-33. doi:10.1016/s2468-1253(24)00317-0

13. De Cruz P, Kamm MA, Hamilton AL, et al. Crohn’s disease management after intestinal resection: a randomised trial. Lancet. Apr 11 2015;385(9976):1406-17. doi:10.1016/s0140-6736(14)61908-5

14. Joustra V, van Sabben J, van der Does de Willebois E, et al. Benefit of Risk-stratified Prophylactic Treatment on Clinical Outcome in Postoperative Crohn’s Disease. J Crohns Colitis. Apr 3 2023;17(3):318–328. doi:10.1093/ecco-jcc/jjac139

15. Ten Bokkel Huinink S, Bak MTJ, Beelen EMJ, et al. The Impact of Postoperative Prophylactic Medication on Long-Term Surgical, Severe Endoscopic and Endoscopic or Radiologic Recurrence Following Primary Ileocecal Resection in Patients With Crohn’s Disease. Aliment Pharmacol Ther. Mar 2025;61(6):1019–1031. doi:10.1111/apt.18496

16. Arkenbosch JHC, Beelen EMJ, Dijkstra G, et al. Prophylactic Medication for the Prevention of Endoscopic Recurrence in Crohn’s Disease: a Prospective Study Based on Clinical Risk Stratification. J Crohns Colitis. Mar 18 2023;17(2):221–230. doi:10.1093/ecco-jcc/jjac128

17. Cohen BL, Fleshner P, Kane SV, et al. Anti-Tumor Necrosis Factor Therapy is Not Associated with Post-Operative Infection: Results from Prospective Cohort of Ulcerative Colitis and Crohn’s Disease Patients Undergoing Surgery to Identify Risk Factors for Postoperative Infection I (Puccini). Gastroenterology. 2019;156(6):S-80. doi:10.1016/S0016-5085(19)36987-2

18. Pouillon L, Remen T, Amicone C, et al. Risk of Late Postoperative Recurrence of Crohn’s Disease in Patients in Endoscopic Remission After Ileocecal Resection, Over 10 Years at Multiple Centers. Clin Gastroenterol Hepatol. Jun 2021;19(6):1218-1225.e4. doi:10.1016/j.cgh.2020.05.027

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Nutrition Reviews in Gastroenterology, SERIES #30

Racial and Ethnic Disparities in Dietary Patterns and Micronutrient Supplementation

March 2026 • Volume MMXXVI, Issue 3
Alexander W. Worix,Edwin McDonald

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Dietary disparities among racial and ethnic minority populations contribute significantly to chronic disease burdens across the lifespan. This review synthesizes evidence on dietary behaviors among middle-aged and older adults, adolescents, and low-income children, highlighting how socioeconomic and structural barriers limit access to healthy foods. Non-Hispanic Black and Latino adults often fall short of fruit and vegetable intake recommendations, while adolescents from low socioeconomic backgrounds demonstrate lower nutritional knowledge and self-efficacy. Children enrolled in supplemental nutrition programs show racial/ethnic disparities in nutrient intake, with Non-Hispanic Black children particularly affected. Supplement use, a potential strategy to reduce nutrient deficiencies, is significantly lower among minority groups, especially women of color. Cultural, educational, and economic factors shape these patterns. Culturally informed nutrition education and policy interventions are needed to address the root causes of these disparities and promote dietary equity. 

Introduction

Racial and ethnic disparities in health outcomes are a persistent concern in the United States, with growing recognition of how social determinants of health, including access to nutritious food and healthcare, add to these inequities. Studies have consistently shown that disparities in dietary patterns and micronutrient intake disproportionately affect racial and ethnic minority populations, contributing to higher rates of chronic diseases, including hypertension, diabetes, obesity, colorectal cancer, and inflammatory bowel disease.1

These disparities are rooted in a complex interplay of structural racism, socioeconomic inequality, food insecurity, limited availability of culturally appropriate dietary guidance, and historical mistrust in the medical system. For example, non-Hispanic Black and Hispanic/Latino populations are more likely to reside in “food deserts,” areas with limited access to affordable, nutritious food, and are less likely to receive adequate counseling on diet and supplementation during medical visits.1 Additionally, variations in cultural norms may further influence dietary practices.

Despite growing awareness of these issues, practical guidance for gastroenterologists and other clinicians on how to address them remains limited. Understanding the causes of underlying dietary disparities is essential for providing equitable, patient-centered care. This review examines the evidence on racial disparities in diet and micronutrient supplementation and offers practical strategies for healthcare providers to reduce these gaps in clinical practice. 

Disparities in Dietary Behaviors of Middle-Aged and Older Adults

Racial and ethnic minorities, particularly non-Hispanic Black individuals, face a disproportionate burden of chronic diseases associated with modifiable lifestyle factors, including cardiovascular disease, hypertension, and diabetes, compared to their White counterparts.1 Diet quality, particularly the consumption of fruits and vegetables, is a key determinant in the prevention and management of these chronic diseases.2 A growing body of evidence from long-term prospective studies demonstrates an inverse relationship between fruit and vegetable intake and the risk of cardiovascular disease, type 2 diabetes, certain cancers, and overall mortality – independent of other health behaviors.3 

Findings on racial and ethnic differences in dietary intake remain mixed. While some studies report that non-Hispanic Black and Latino middle-aged and older adults consume fruits and vegetables at levels comparable to non-Hispanic Whites,4 other research has shown significantly lower intake among non-Hispanic Black adults.5 August et al. reported that non-Hispanic White adults were more likely to engage in a range of health-promoting behaviors compared to their racial/ethnic minority counterparts during middle adulthood, although these differences were less pronounced in later life.1 Notably, among adults aged 45-64 years, only English-proficient Latino respondents were significantly less likely to meet daily fruit and vegetables recommendations compared to Whites. Among adults aged greater than 65 years, both non-Hispanic Black and limited English-proficient Latino respondents had significantly lower odds of meeting recommended intake levels.2 These findings are consistent with previous literature documenting lower fruit and vegetable consumption among Black adults relative to Whites.6 These findings also suggest that acculturation, including English language proficiency, may impact the dietary behaviors of non-White Hispanic adults. 

Adolescent Dietary Behavior and the Role of School-Based Interventions

Obesity represents the second leading cause of preventable death and is a key contributor to chronic diseases such as cardiovascular disease and cancer in the United States.7 Over recent decades, obesity prevalence has risen sharply, particularly among youth. Rates have tripled among children age 6-11 years and doubled among adolescents aged 12-19 years.7 Overweight children are more likely to become overweight in adulthood, placing them at elevated risk for future morbidity and mortality due to chronic disease. One contributor to this trend is the increasing consumption of food prepared away from home, which has been associated with higher intake of empty calories from sugar-sweetened beverages, elevated  saturated fat consumption, and increased sodium intake.8 Concurrently, this dietary pattern is linked to reduced intake of nutrient-rich foods, including fruits, vegetables, and fiber.8 

Adolescents from low socioeconomic status (SES) backgrounds are particularly vulnerable to suboptimal dietary habits, with studies consistently showing lower consumption of fruits and vegetables and greater intake of refined sugars and fats compared to peers from higher SES backgrounds. Low SES is also associated with increased morbidity, including hypertension, osteoarthritis, and asthma, and higher mortality due to chronic diseases such as cardiovascular disease and cancer.9 

Fahlman et al. conducted one of the first studies to examine dietary behaviors, nutritional knowledge, and self-efficacy among a large cohort of non-Hispanic Black students from low SES backgrounds compared to non-Hispanic White students from higher SES backgrounds.10 The findings revealed significant disparities across all domains, showing that non-Hispanic Black Students from low SES backgrounds demonstrated markedly poorer dietary behaviors (Table 1).10 Several factors may contribute to these disparities, including limited access to healthy foods, financial constraints, and reduced exposure to nutrition education.10 Notably, lower SES families often reside in neighborhoods with a high density of fast-food restaurants and few grocery stores offering affordable, fresh produce.10

Table 1. Dietary Behaviors and Knowledge and Knowledge by SES and Race10

VariableBlack Students
(Low SES)		White Students
(High SES)		p-Value
Daily fruit intakeLowerHigher<0.001
Daily vegetable intakeLowerHigher<0.001
Empty calorie consumptionHigherLower<0.001
Knowledge of dietary guidelinesLowerHigher<0.001
Belief in ability to eat healthfullyLowerHigher<0.001
Confidence in eating healthy at fast-foodLowerHigher<0.001

Table 2. Impact of Nutrition Education Programs on Dietary Knowledge and Self-Efficacy

StudyPopulationIntervention DetailsOutcome
Fahlman et al.14Black middle school students8-session programIncrease fruit/vegetable intake, increase confidence in
healthy choices
Auld et al.15Hispanic students (K-12)16 weekly lessonsIncrease confidence to eat 5+ servings of fruits/vegetables
per day
Lytle et al.13,16Diverse student populationsYear-long school-based interventionDecrease total fat/saturated fat intake, increase nutrition knowledge 

Nutritional knowledge is a modifiable factor that strongly influences adolescent dietary behaviors. Fahlman et al. found that non-Hispanic Black students from low SES backgrounds were less knowledgeable about basic nutritional guidelines (Table 1).10,11 Self-efficacy, the belief in one’s ability to perform a specific behavior, is another key determinant of health behavior. It was reported that non-Hispanic Black students of low SES were less confident in their ability to adopt healthy eating behaviors (Table 1).10 However, self-efficacy, like knowledge, can be improved through structured interventions. School-based nutrition education programs have demonstrated efficacy in increasing knowledge across diverse student populations and have shown improvement in students’ overall dietary self-efficacy (Table 2).12-15 

Table 3. Racial/Ethnic Differences in Nutrient Intake Among Children Participating in WIC (NHANES 2011–2014)17

NutrientHispanic vs Non-Hispanic WhiteNon-Hispanic Black vs
Non-Hispanic White		Notes
FiberHigher (p=0.026)—Hispanic children had greater fiber intake
PotassiumHigher (p=0.038)—Hispanic children had greater potassium intake
Calcium—Lower (p=0.009)Non-Hispanic Black children had lower intake
Vitamin D—Lower (p=0.012)Non-Hispanic Black children had lower intake
Sodium—Higher (p=0.006)Non-Hispanic Black children had higher intake
Saturated Fat—Lower (p=0.0016)Non-Hispanic Black children had lower intake

Although changing actual dietary behavior is more complex than improving knowledge or self-efficacy, multiple school-based programs have demonstrated meaningful behavioral change. Studies found reductions in saturated and total fat intake after a year-long intervention, with benefits observed across all racial groups (Table 2).16 Increased fruit and vegetable intake among elementary and middle school students following shorter, curriculum-based interventions have also been reported.12-14

Dietary Intake of Children in the United States Participating in WIC

The Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) represents a critical opportunity to improve access to nutritious foods in low-income households and to mitigate diet-related health disparities.17 WIC food packages include provisions for grains, fruits, and vegetables, dairy and protein sources. Studies have identified nutrient inadequacies and excesses linked to adverse health outcomes in WIC populations, informing subsequent revisions to the WIC food package.18,19 However, these reviews rarely addressed racial and ethnic disparities. 

Zimmer et al. analyzed data from national databases to assess differences in nutrient and food group intake among WIC participants by race/ethnicity.17 In this nationally representative cohort of WIC-participating children, significant racial and ethnic disparities in nutrient intake were observed. Compared to non-Hispanic White children, Hispanic children had diets with lower energy density and more favorable nutrient profiles (including higher intake of fiber and potassium) (Table 3).17 In contrast, non-Hispanic Black children exhibited poorer nutrient intake profiles (except for higher intake of sodium), compared to their non-Hispanic White counterparts.17 These disparities are concerning given the well-established link between high sodium intake and hypertension, which disproportionately impacts the non-Hispanic Black population.20 Notably, non-Hispanic Black children reported lower saturated fat intake, representing one area of relative dietary advantage (Table 3).17 Despite these differences, mean nutrient intakes among WIC-participating children across all racial and ethnic groups fell short of several dietary recommendations.17

Analysis of food group intake revealed additional disparities. non-Hispanic Black children consumed significantly less dairy compared to non-Hispanic White children, a finding that may be partially explained by higher reported rates of lactose intolerance among Black Americans.17,21 Total protein consumption was higher among both non-Hispanic Black and Hispanic children compared to non-Hispanic White children.17 Across all racial and ethnic groups, mean intakes for key food groups such as seafood, total vegetables, whole grains, nuts and seeds, total dairy, and legumes were below recommended levels when converted to a daily intake basis.17, 22

Zimmer et al. emphasized the potential for WIC nutrition education efforts to address these disparities. For example, promoting the use of lactose-free alternatives, such as fortified non-dairy yogurts and cheeses, could help improve dairy intake and related nutrient deficiencies among non-Hispanic Black children.17 Future WIC interventions should integrate food package changes, nutrition education, and equity-focused strategies to reduce racial disparities and overall, to improve nutrition health.17 

Nutrient Deficiencies and the Contribution of Dietary Supplements in Racial and Ethnic Population Subgroups

Adequate intake of essential nutrients is critical for maintaining optimal health. Nevertheless, many Americans fall short of meeting the recommended nutrient intake levels. Dietary supplement use has been shown to increase overall nutrient intake and reduce the prevalence of nutrient inadequacy.23,24 The Dietary Guidelines for Americans 2015-2020 (DGA) recommend a dietary pattern rich in nutrient-dense foods, and in some cases, the use of fortified foods and dietary supplements to help achieve recommended intakes.25 The Dietary Guidelines identify potassium, dietary fiber, choline, magnesium, calcium, iron (for certain age/gender groups), and vitamins A, D, E, and C as “under consumed nutrients.” Vitamin D, calcium, potassium, and fiber are further classified as “nutrients of public health concern” due to their association with increased chronic disease risk when underconsumed.21 Dietary supplement use has risen over time in the United States, with approximately 50% of adults reporting supplement use, and two-thirds of users reporting intake of multivitamin-multimineral supplements.22,24  

Nutrient deficiencies have been associated with increased risks of adverse health outcomes, including cardiovascular disease, stroke, cognitive impairment, certain cancers, visual disorders, and poor bone health. Recent analyses of the National Health and Nutrition Examination Survey (NHANES) 2009-2012 data revealed a range of micronutrient inadequacies among U.S. racial and ethnic groups.26 Differences in key nutrient consumption may contribute to disparities in diet-related chronic diseases observed among racial/ethnic groups. 

Blumberg et al. highlighted significant racial/ethnic differences in supplement use, with non-Hispanic Whites reporting higher rates of supplement use compared to other racial/ethnic groups.26,27 These findings may contribute to higher overall nutrient intake and a lower prevalence of nutrient inadequacy among non-Hispanic Whites. The usual intakes of DGA-identified under consumed nutrients varied significantly across racial/ethnic groups, with observed mean intake differences favoring non-Hispanic Whites in all key nutrients (Table 4).26 Moreover, the proportion of individuals with intakes below the Estimated Average Requirement (EAR) and prevalence of inadequacy was significantly lower among non-Hispanic Whites in almost all key nutrients compared to other racial/ethnic groups.26 

These findings are consistent with previous studies that demonstrated significantly lower intakes of several under consumed and public health concern nutrients among non-Hispanic Black and Hispanic populations compared to non-Hispanic Whites.27 Lower intakes of these nutrients may contribute to the disparities in diet-related chronic disease observed among minority populations.28,29 

Cultural and Demographic Influence on Supplement Use Among Minority Women

Women of African American, Hispanic, Asian, Pacific Islander, Native American, and Alaskan Native descent represent approximately 29% of the female population in the United States; however, they continue to experience disproportionately greater health burdens compared with non-Hispanic White women.30 For example, regular use of multivitamin supplements has been associated with a reduced risk of congenital birth defects, coronary artery disease, colon cancer, and breast cancer, particularly among individuals who consume alcohol.30 Despite these benefits, studies identified that supplement use is most prevalent among older, well-educated, higher-income, non-Hispanic White women, particularly those residing in the western United States.30,31 This demographic trend highlights an important disparity: women who might benefit the most from supplementation are often those least likely to use these products. 

Research from iron and folic acid supplementation programs in developing countries suggests that diverse cultural practices, attitudes, and beliefs influence supplement use behaviors.30 However, in the United States, there is a paucity of literature exploring how cultural and ethnic factors shape supplement use patterns. Jasti et al. sought to address this knowledge gap by investigating supplement use behaviors among women of various ethnic backgrounds.30 Studies also examined health knowledge and attitudes among female supplement users. It was noted that a significantly higher proportion of White women reported supplement use compared to women of different racial/ethnic groups (Table 5).32 In contrast, women from minority backgrounds had poorer health knowledge and attitudes about dietary supplementation.32

Ethnographic studies on iron and folic acid supplementation programs among women of reproductive age in developing countries offer valuable insights.30 For example, in Malawi, Coca-Cola was commonly believed to “increase blood” and was often preferred over iron tablets despite its higher cost.33 Additionally, fears that iron tablets could cause “too much blood” and activate dormant illnesses were prevalent.33 In Indonesia and Honduras, women expressed concerns that iron tablets could lead to weight gain or fetal deformities.34 In India, symptoms such as fatigue, weakness, and dizziness were often normalized as part of a typical pregnancy, delaying recognition and treatment of anemia.35 These findings underscore the powerful influence of cultural beliefs on health behaviors and highlight the importance of culturally sensitive public health messaging. 

Table 4. Differences in Nutrient Inadequacy Across Racial and Ethnic Groups (NHANES 2009–2012)26

NutrientGreatest Prevalence
of Inadequacy		Lowest Prevalence
of Inadequacy		Range of Differences
in Usual Intake (%)
CalciumHispanic, NH-BlackNH-White8–20%
IronHispanicNH-White11–21%
Vitamin ANH-BlackNH-White34–55%
Vitamin CNH-BlackNH-White42–114%
Vitamin DNH-BlackNH-White82–218%
Vitamin EHispanic, NH-BlackNH-White129–236%
MagnesiumHispanic, NH-BlackNH-White14–35% (lower prevalence)
Vitamin KNH-Black, HispanicNH-WhiteNot quantified, but higher intake in NH-Whites

Table 5. Health Knowledge and Attitudes Among Female Supplement Users32

CharacteristicNon-Hispanic White WomenWomen of Other Racial/Ethnic Groups
Reported supplement useSignificantly higherLower
Chronic disease diagnosis among usersMore likelyLess likely
Belief that diet influences disease riskMore likelyLess likely
Belief that weight is modifiableMore likelyLess likely – often viewed as unmodifiable
Adoption of health-promoting behaviorsMore proactiveLess proactive

Acculturation and Dietary Patterns

In the United States, low SES is associated with poor child health outcomes—including impaired growth and development. Hispanic families, for instance, are disproportionately affected by poverty compared to non-Hispanic white families (18.5% and 5.3%, respectively).36 This discrepancy may, in part, be explained by acculturation. Acculturation is a complex, long-term process in which individuals adopt and modify cultural values, norms, and behaviors, including those related to diet and lifestyle. The degree of linguistic, social, cultural, and economic assimilation among immigrant parents shapes their children’s acculturation experience and, consequently, their health and well-being. Importantly, acculturation-related changes have been linked to increased risks of obesity and chronic disease due to altered eating patterns—such as higher caloric intake, more frequent snacking, and reduced physical activity.37

Mazur et al. demonstrated that parental language use, a proxy for acculturation, was associated with differences in dietary intake. Specifically, exclusive use of Spanish correlated with variations of energy, protein, sodium, and folate consumption, as well as percentages of energy derived from fat and saturated fat.38 Although not significant for all indicators, patterns consistently revealed that food insecurity decreased with lower acculturation (odds ratio [OR]: 0.4; 95% CI: 0.2, 0.7 for adult meal size reduction) but increased with poverty (OR: 5.9 [3.0, 11.7] and 5.4 [2.2, 13.4] for reduced child meal size).38 These findings underscore that both acculturation and economic hardship play crucial roles in shaping children’s diets and household food insecurity. 

Table 6. Acculturation and Socioeconomic Influence on Nutritional Disparities

DomainKey Findings
OverviewNutritional disparities across racial, ethnic, and socioeconomic groups stem from both cultural and structural factors.
Socioeconomic StatusLow income is linked to poorer child health; Hispanic families experience higher poverty (18.5%) than non-Hispanic White families (5.3%).
AcculturationThe process of adopting new cultural norms influences diet and lifestyle behaviors. Higher acculturation is associated with increased caloric intake, snacking, and reduced physical activity.
Parental Language and DietLanguage use reflects acculturation level; exclusive Spanish use corresponds with distinct nutrient patterns (energy, sodium, folate, fat composition).
Food SufficiencyLower acculturation is associated with less food insufficiency, while poverty substantially increases food insecurity and meal reduction.
Public Health ImplicationsInterventions should integrate culturally responsive education with strategies to improve economic stability.

Table 7. Summary of Ultra-Processed Food Consumption and Related Disparities in the United States

DomainKey Findings
DefinitionIndustrially formulated, ready-to-eat products combining food-derived ingredients and additives to enhance taste, convenience, and shelf life.
PrevalenceAbout 43% of packaged food and beverage purchases in the U.S. are ultra-processed.
Socioeconomic PatternsLower income and education groups purchase the highest proportion of UPFs; higher income and education groups purchase the least.
Dietary TrendsLower-income households consume more UPFs and fewer fruits and vegetables; higher-income households show healthier purchasing patterns.
Health EffectsHigh UPF intake is linked to increased risk of cardiovascular disease, cancer, obesity, and all-cause mortality.
Hypertension RiskGreater UPF intake (by calories or grams) increases hypertension risk. Associations differ by race — stronger among Black adults when measured by grams, suggesting higher total UPF intake.
Mediating FactorsBody mass index and dietary quality partly explain UPF–hypertension relationships, varying by racial group.
Social DeterminantsUPFs’ low cost, convenience, and energy density make them prevalent in economically constrained settings; structural inequities further reinforce these consumption patterns.

Food Insecurity in Neighborhood Food Environments

Food insecurity and limited access to affordable, nutritious foods are strongly linked to poor diet quality and elevated risks of cardiovascular disease, diabetes, and certain cancers.39 Populations with lower SES and racial or ethnic minority groups face disproportionately high rates of food insecurity and are more likely to reside in under-resourced food environments.40 Approximately 13.5 million people in the United States live in areas with limited access to supermarkets or large grocery stores, restricting their ability to purchase fresh, healthy foods.

Recent longitudinal analyses have shown that higher diet quality correlates with greater proximity to and density of food stores, neighborhood SES, and perceptions of healthy food environment. These associations are even stronger among racial and ethnic minority populations.41 Moreover, studies have found that residing in neighborhoods with limited grocery access and high fast-food density is associated with increased risks of hypertension, cardiovascular diseases, diabetes, and lower cancer survival.42 

Despite decades of research, substantial gaps remain in our understanding of the pathways linking food insecurity and neighborhood food environments to racial, ethnic, and socioeconomic disparities in health outcomes. Social determinants of health, such as food insecurity and access to affordable, nutritious food are themselves shaped by structural determinants—policies, systems, and distributions of resources that reflect structural racism and socioeconomic inequity. These structural factors interact with cultural norms, traditions, and values to shape dietary behavior.43

Ultra-Processed Foods, Socioeconomic Disparities, and Nutrition-Related Chronic Disease in the United States

American diets are increasingly dominated by ultra-processed foods (UPFs). UPFs are defined as ready-to-eat industrial products formulated from food-derived ingredients combined with additives through multiple industrial processes, designed primarily to enhance palatability, convenience, and profitability.44 Mounting evidence links UPF consumption to the global rise in diet-related chronic diseases—including cardiovascular disease, cancer, obesity, and all-cause mortality.45 

Racial, ethnic, and income disparities in obesity and nutrition-related chronic disease are well documented in the United States. Differences in dietary intake and purchasing patterns across demographic groups may contribute substantially to these inequities (Table 7).44 Dunford et al. reported that 43% of barcoded packaged foods and beverage purchases from U.S. grocery stores in 2020 were derived from UPF.44 When stratified by SES and educational status, the lowest income and education groups (high school) had the highest proportion of purchases from UPFs, whereas the highest income and education groups (college degree) had the lowest.44 These findings align with prior research showing that lower-income households consume a greater proportion of UPFs and fewer nutrient-dense foods such as fruits and vegetables, while higher-income households demonstrate healthier purchasing behaviors, including fewer processed meats and sugar-sweetened beverages.46 

Oladele et al. further demonstrated that diets with a greater proportion of calories and grams from UPFs are associated with increased risk of incident hypertension.47 Notably, race-stratified analyses revealed differences in the strength and nature of this association among Black and White adults. When UPF intake was expressed as percent kilocalories, associations were statistically significant only among White adults.47 In contrast, when UPF was expressed as percent grams, strong positive associations were observed among Black adults.47 These findings suggest that the greater hypertension risk observed in Black adults when measured by grams may reflect higher total UPF consumption, including low-calorie UPFs, compared with white adults.47 Post hoc analyses confirmed higher mean UPF intake (in grams) among Black adults. The study also identified differential mediation by body mass index (BMI) and dietary quality in the relationship between UPF intake and incident hypertension across racial groups.47  

Beyond biological mechanisms, social and structural determinants play a crucial role in shaping UPF consumption patterns. UPFs are typically inexpensive, shelf-stable, ready-to-eat, and energy-dense—characteristics that make them accessible and appealing to consumers, particularly in economically constrained settings.47 Structural inequities in housing, employment, and access to health-promoting resources further exacerbate these patterns. Limited access to affordable, high-quality foods and greater exposure to calorie-dense, ultra-processed options contribute to persistent nutritional disparities.48 

Strategies to Bridge Gaps

Practical strategies to bridge these gaps include integrating culturally sensitive nutrition education and counseling into clinical practice, supporting community-based and school-based dietary interventions, promoting policy changes to expand access to healthy foods, and encouraging appropriate use of dietary supplements where food-based strategies are insufficient. Gastroenterologists and other healthcare providers must recognize the role of structural determinants in shaping dietary behaviors and proactively engage with patients from diverse backgrounds to deliver equitable, patient-centered nutritional care (See Box 1). Future research should prioritize interventions that not only improve dietary intake across racial and ethnic groups but also address the broader systemic factors that perpetuate nutritional inequities. 

Box 1. Practical Guidelines for Clinicians — Addressing Racial and Ethnic Disparities in Diet and Nutrition

1. Conduct Culturally Informed Nutritional Assessments
– Include cultural food practices and preparation methods in dietary histories.
– Screen for common micronutrient deficiencies more prevalent in specific populations.

2. Identify Structural Barriers to Healthy Eating –
Screen for food insecurity using tools like the Hunger Vital Sign™.
– Be aware of patients’ access limitations due to cost, transportation, or neighborhood food environments.
– Refer to local resources (e.g., SNAP, WIC, food pantries).

3. Deliver Tailored Nutrition Education and Counseling
– Customize guidance to reflect cultural preferences and socioeconomic realities.
– Promote healthy adaptations of traditional meals.
– Use interpreters and translated materials as needed.

4. Promote Appropriate Use of Nutritional Supplements
– Recommend supplements only when clinically indicated.
– Encourage a food-first approach, considering patients’ access to nutrient-rich foods.

5. Engage with Community and Institutional Resources
– Partner with local organizations to support community-based nutrition programs.
– Advocate for integrated dietitian services within GI practices.

6. Advocate for Policy-Level Change
– Support policies that improve food access, restrict targeted marketing of unhealthy foods, and expand coverage for nutritional counseling.

7. Build Trust Through Culturally Responsive Care
– Acknowledge systemic contributors to mistrust.
– Prioritize shared decision-making and respect for cultural values.

8. Commit to Lifelong Learning and Research
– Stay current on nutrition disparities research.
– Participate in or support research that explores nutrition-related outcomes across diverse groups.

Conclusion

Racial and ethnic disparities in diet quality, micronutrient intake, and dietary supplement use are well-documented contributors to health inequities across the lifespan. These disparities are rooted in complex socioeconomic, structural, and cultural factors that influence access to nutritious foods, dietary behaviors, and health outcomes. Middle-aged and older adults from minority groups face disproportionate burdens of diet-related chronic disease, while adolescents from low-income, minority backgrounds often experience early nutritional deficits that set the stage for lifelong health risks. Participation in nutrition assistance programs like WIC offers critical opportunities to address disparities; however, gaps in nutrient intake persist and vary by race and ethnicity. Furthermore, differences in dietary supplement use amplify existing disparities in nutrient adequacy, underscoring the need for tailored interventions.  

References

References
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12. Powers AR, Struempler BJ, Guarino A, Parmer SM. Effects of a nutrition education program on the dietary behavior
and nutrition knowledge of second-grade and third-grade students. J Sch Health. 2005;75(4):129-133.

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15. Auld GW, Romaniello C, Heimendinger J, Hambidge C, Hambidge M. Outcomes from a school-based nutrition education program alternating special resource teachers and classroom teachers. J Sch Health. 1999;69(10):403-408.

16. Lytle LA, Stone EJ, Nichaman MZ, et al. Changes in nutrient intakes of elementary school children following a schoolbased intervention: results from the CATCH Study. Prev Med. 1996;25(4):465-477.

17. Zimmer MC, Rubio V, Kintziger KW, Barroso C. Racial/ Ethnic Disparities in Dietary Intake of U.S. Children Participating in WIC. Nutrients. 2019;11(11):2607.

18. National Academies Press. Review of WIC Food Packages; National Academies Press: Washington, DC, USA, 2017.

19. Zimmer MC, Vernarelli JA. Changes in nutrient and food group intakes among children and women participating in the Special Supplemental Nutrition Program for Women, Infants, and Children: findings from the 2005-2008 and 2011-2014 National Health and Nutrition Examination Surveys. Public Health Nutr. 2019;22(18):3309-3314.

20. Musemwa N, Gadegbeku CA. Hypertension in African Americans. Curr Cardiol Rep. 2017;19(12):129.

21. Nicklas TA, Qu H, Hughes SO, et al. Self-perceived lactose intolerance results in lower intakes of calcium and dairy foods and is associated with hypertension and diabetes in adults. Am J Clin Nutr. 2011;94(1):191-198.

22. Briefel RR, Johnson CL. Secular trends in dietary intake in the United States. Annu Rev Nutr. 2004;24:401-431.

23. Fulgoni VL 3rd, Keast DR, Bailey RL, Dwyer J. Foods, fortificants, and supplements: Where do Americans get their nutrients? J Nutr. 2011;141(10):1847-1854.

24. Bailey RL, Gahche JJ, Lentino CV, et al. Dietary supplement use in the United States, 2003-2006. J Nutr. 2011;141(2):261-266.

25. U.S. Department of Health and Human Services; U.S. Department of Agriculture. 2015–2020 Dietary Guidelines for Americans. 8th Edition. December 2015.

26. Blumberg JB, Frei B, Fulgoni VL III, Weaver CM, Zeisel SH. Contribution of Dietary Supplements to Nutritional Adequacy in Race/Ethnic Population Subgroups in the United States. Nutrients. 2017;9(12):1295.

27. Bowman SA. Socioeconomic characteristics, dietary and lifestyle patterns, and health and weight status of older adults in NHANES, 1999 2002: a comparison of Caucasians and African Americans. J Nutr Elder. 2009;28(1):30-46.

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30. Jasti S, Siega-Riz AM, Bentley ME. Dietary supplement use in the context of health disparities: cultural, ethnic and demographic determinants of use. J Nutr. 2003;133(6):2010S-2013S.

31. Balluz LS, Kieszak SM, Philen RM, Mulinare J. Vitamin and mineral supplement use in the United States. Results from the third National Health and Nutrition Examination Survey. Arch Fam Med. 2000;9(3):258-262.

32. Tippet KS, Cypel YS. (1997) Design and Operation: The Continuing Survey of Food Intake by Individuals and the
Diet and Health Knowledge Survey 1994–96. Nationwide Food Surveys Report 96–1. United States Department of Agriculture, Agricultural Research Service.

33. Williams L, Semu L, Behague D, Sibale C, France C. (1996) A qualitative study of constraints to reducing iron deficiency and anaemia in women of reproductive age in Thyolo district, Malawi. Arlington, VA: MotherCare, John Snow Inc.

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37. Kaiser LL, Melgar-Quiñonez HR, Lamp CL, Johns MC, Harwood JO. Acculturation of Mexican-American mothers influences child feeding strategies. J Am Diet Assoc. 2001;101(5):542-547.

38. Mazur RE, Marquis GS, Jensen HH. Diet and food insufficiency among Hispanic youths: acculturation and socioeconomic factors in the third National Health and Nutrition Examination Survey. Am J Clin Nutr. 2003;78(6):1120-1127.

39. Gundersen C, Ziliak JP. Food Insecurity And Health Outcomes. Health Aff (Millwood). 2015;34(11):1830-1839.

40. Coleman-Jensen A., Rabbitt M.P., Gregory C.A., Singh A. Household food security in the United States. Economic Research Report. 2022:155.

41. Gao X, Engeda J, Moore LV, Auchincloss AH, Moore K, Mujahid MS. Longitudinal associations between objective and perceived healthy food environment and diet: The Multi-Ethnic Study of Atherosclerosis. Soc Sci Med. 2022;292:114542.

42. Kanchi R, Lopez P, Rummo PE, et al. Longitudinal analysis of neighborhood food environment and diabetes risk in the Veterans Administration diabetes risk cohort. JAMA Netw Open. 2021;4(10):e2130789.

43. Odoms-Young A, Brown AGM, Agurs-Collins T, Glanz K. Food Insecurity, Neighborhood Food Environment, and Health Disparities: State of the Science, Research Gaps and Opportunities. Am J Clin Nutr. 2024;119(3):850-861.

44. Dunford EK, Miles DR, Popkin BM. Exploring disparities in the proportion of ultra-processed foods and beverages purchased in grocery stores by US households in 2020. Public Health Nutr. 2025;28(1):e85.

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46. Lacko AM, Maselko J, Popkin B, Ng SW. Socio-economic and racial/ethnic disparities in the nutritional quality of packaged food purchases in the USA, 2008-2018. Public Health Nutr. 2021;24(17):5730-5742.

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48. Odoms-Young A, Bruce MA. Examining the Impact of Structural Racism on Food Insecurity: Implications for Addressing Racial/Ethnic Disparities. Fam Community Health. 2018;41 Suppl 2 Suppl, Food Insecurity and Obesity(Suppl 2 FOOD INSECURITY AND OBESITY):S3-S6.

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Frontiers in Endoscopy, Series #104

Boerhaave Syndrome: An Updated Review with an Emphasison Endoscopic Treatments

March 2026 • Volume MMXXVI, Issue 3
Taranika Sarkar Das,Douglas G. Adler

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Introduction 

Spontaneous rupture of the esophagus is also known as Boerhaave syndrome after the Dutch physician who first described it in 1724.1 Historically, Boerhaave syndrome was considered uniformly fatal.

Boerhaave syndrome is a rare entity and is typically seen in middle-aged men after heavy food or alcohol intake, occurring in about 3 per 1,000,000 patients per year.2

The sudden rise of intraesophageal and intraabdominal pressure against a closed glottis creates a severe pressure gradient across the mediastinum, where the intrathoracic pressure gradient is very low during retching. This, along with dyssynergia between the upper and lower esophageal sphincters, produces a wall stress that results in a full thickness tear – usually occurring along the left posterolateral distal esophagus at the level of the gastroesophageal junction. (Figure 1) Subsequent leakage of luminal contents into the surrounding tissue, if untreated, leads to sepsis, organ failure, and death.3,4

Classically, Boerhaave syndrome presents as Mackler’s triad: vomiting, chest pain, and subcutaneous emphysema.5 One-third of patients present atypically.5 Mortality has historically been high and often ranges from 15% to 42%, but is lower in the modern era.6,7

There has been a paradigm shift in the management of Boerhaave syndrome over the last decade. Earlier, the disorder was treated exclusively with surgery; however, it is now managed with a multidisciplinary approach and thoracic surgical interventions are rarely needed. The overall prognosis is largely determined by prompt diagnosis and treatment. Survival falls dramatically when treatment is delayed beyond 24 hours.8

The Pittsburgh Esophageal Perforation Severity Score (PSS) was originally validated for all causes of esophageal perforation and is a useful tool to stratify risk.9 The score was seen to perform particularly well in the Boerhaave syndrome subgroup (119) in a multinational multicenter retrospective cohort study (1990-2014), done on 288 adults with esophageal perforation.

The PSS assigns points to clinical variables for a maximum score of 18 and classifies patients as low risk (<2), intermediate risk (2–5), or high risk (>5) for death and major complications. Higher PSS values correlate with longer diagnostic delay, favors operative rather than conservative management, predicts increased need for ICU care, prolonged length of hospital stay, and higher in-hospital mortality.10 These findings were corroborated in a retrospective single-center cohort of 56 patients, 21.4% of whom had Boerhaave syndrome.11

Other Esophageal Conditions Predisposing to Boerhaave Syndrome 

Boerhaave syndrome may arise in an esophagus that is structurally or functionally abnormal as can be seen in patients with achalasia, eosinophilic esophagitis (EOE), benign strictures, malignancy, and esophageal varices.12 These underlying conditions affect treatment selection and prognosis. In patients with EOE, chronic inflammation leads to remodeling which weakens the esophageal wall and predisposes the patient to transmural rupture.13 On the other hand, high intraluminal pressures along with impaired emptying in patients with achalasia, predispose the esophagus to rupture spontaneously.14

Atypical and High-Risk Presentation in Boerhaave Syndrome 

Atypical and high-risk presentations often occur in older or patients with comorbidities. In a retrospective series on 18 hospitalized patients in Turkey, up to one-third of esophageal perforations were initially misdiagnosed as acute coronary syndrome, pulmonary embolism, aortic dissection, perforated peptic ulcer, pancreatitis, pneumonia, or acute hepatitis. This led to delays in definitive treatment and higher mortality.15 A multicenter study in Belarus on 103 hospitalized patients 31 % of the patients were misdiagnosed initially as perforated peptic ulcer, pneumonia, pancreatitis, or acute hepatitis. Several patients underwent unnecessary laparotomy or other procedures.16

Physical Exam/Prognosis and Diagnosis 

The majority of patients with Boerhaave syndrome present with chest pain. Other signs may include fever, dyspnea, diaphoresis, and subcutaneous or mediastinal emphysema. Up to one-fifth of cases are initially misdiagnosed.16 Various studies have determined the prognostic factors for Boerhaave syndrome. Older age, significant comorbidities, leukopenia, high CRP, larger tears, thoracic abscess or pleural contamination, overt sepsis, high ASA class and delayed treatment were consistently associated with worse outcomes.18-20 

Diagnosis

Retrospective studies support CT-based strategies as first-line imaging. It has a near-100% sensitivity and negative predictive value for ruling out perforation.21,21 CT-esophagography has been shown to be an excellent tool to rule BS in prospective series.23,24 It directly shows contrast leaks and peri-esophageal collections. Water-soluble contrast esophagography remains a useful complementary test, especially to clarify equivocal CT findings.25

Management

Historically Boerhaave syndrome has been managed almost entirely with urgent open surgery (primary repair or esophagectomy plus wide pleuro-mediastinal drainage). Early primary repair was associated with reduced leaks, but was maximally invasive and irreversible.26-28 Modern management has shifted to a multimodal, minimally invasive approach with surgery being reserved for a small minority of cases. In a retrospective cohort study on 80 patients in Germany, patients treated via endoscopic approaches achieved similar survival with less morbidity compared to those who underwent emergency surgery.26

Thoracoscopic/laparoscopic/trans-hiatal approaches are far less frequently employed today, with most patients undergoing endoscopic management as first line therapy.29,30 

Stents

Stents have been used for Boerhaave syndrome dating back to 2001.32 Fully covered and partially covered metal stents as well as plastic esophageal stents have been used (although plastic esophageal stents are now obsolete). (Figures 2 and 3) A systematic review and meta-analysis in 2024 across 18 observational studies on 171 patients with spontaneous esophageal perforations (mostly Boerhaave syndrome patients) reported that closure was achieved in 90/110 patients (82%). In the weighted pooled analysis, the closure rate was 86% (95% CI 77-93%). In the same analysis, failure with stents was reported for 27/160 (17%) with a pooled failure rate of 14% (95% CI 7-22%). Weighted mortality was 6% (95% CI 2–13%).33 

In a more recent single center study from Norway that reported on 17 consecutive patients with Boerhaave syndrome (2015-2022), overall outcomes were good. 14 self-expanding metal stents (SEMS) including 12 partially covered and 2 fully covered were utilized. Perforations sealed initially with stent alone in 10, endoscopic vacuum therapy (EVT) alone in 3, and combined stent and EVT in 4 patients. All defects were endoscopically sealed within 12 h of arrival. Mortality was reported only in one patient, however complete endoscopic healing was reported in all surviving patients. 

With regards to adverse events, early leakage was reported in 10 patients and 4 patients needed repeat stenting for persistent leaks. Stent migration was reported in 4 patients. Long term adverse events included stricture formation in three patients. Transthoracic drainage via IR was needed in 15/17 patients.34

In a single-center retrospective series from a Dutch tertiary referral center on 21 consecutive Boerhaave syndrome patients, stent-related adverse occurred in 7/19 (37%) stented patients; 3 of these 7 were migrations (two required endoscopic repositioning, one removal).35

Delayed stent migration has been reported as well with a case report of tracheoesophageal fistula forming after multiple stent placements, perforations, diversion, and gastric pull-up for Boerhaave syndrome.36 Another case of small bowel obstruction was seen in a patient with Boerhaave syndrome who was treated with a fully covered esophageal metal stent that had migrated to the jejunum.37

EVT 

Endoscopic vacuum therapy (EVT) makes use of continuous negative pressure to drain and collapse an esophageal defect so it can granulate and heal. There are two types of EVT. One is the classic open-pore polyurethane foam, commercially available as Eso-SPONGE / Endo-SPONGE (Boston Scientific, Massachusetts, U.S.A.), the other is an open-pore film sponge (OFD), commercially available as Suprasorb (Lohmann & Rauscher International GmbH & Co. KG, Rengsdorf, Germany). The Endo-SPONGEis mounted on a nasogastric or drainage tube. Then it is placed endoscopically either inside the esophageal lumen across the defect or in the peri-esophageal cavity. A vacuum pump (typically –80 to –150 mmHg) is connected to either of the tubes. It provides constant suction that evacuates pus and secretions, and stimulates granulation and reepithelization. The device needs to be exchanged every 2–4 days until the cavity has collapsed.38 OFD uses a thin open-pore drainage film wrapped around a nasogastric tube, which is often double lumen in design. Its smaller diameter can be passed through narrow strictures or be placed nasally. One lumen is connected to suction and the other can be used for feeding or decompression.39

The first use of EVT to treat patients with Boerhaave syndrome was reported in Germany in 2014. Heits et al. published a single center retrospective series on 10 patients with benign esophageal perforation including 5 Boerhaave syndrome patients who were treated with EVT as the first line therapy. They used the Endo-Sponge system with a of mean 5.4 sessions (2-12) over 19 days. Six patients started EVT within 24 h and four started after 24 h. Delayed initiation of treatment was associated with significantly longer EVT duration and hospital stay. Complete endoscopic healing was seen in 8/10 patients. Failure was reported in two patients with one requirement placement of a covered stent to speed closure. Hospital mortality was 10% though the cause was from cardiovascular collapse after successful EVT. 8/10 patients required pleural drainage either with IR or video-assisted thoracoscopic surgery (VATS). The authors strongly advocated the routine use of CT after placement to look for fluid collections that would warrant additional external drainage.38

Loske et al. used EVT to demonstrate a complete, organ preserving closure in a patient with Boerhaave syndrome. They started with the standard open-pore polyurethane foam drains; then when the perforation had shrunken to a narrow canal, they switched to OFD, allowing continued EVT through the tiny opening.40 A similar case highlighted EVT’s role as a salvage modality after failed primary closure and T-tube drainage.41

A systematic review and meta-analysis analyzing the efficacy and safety of EVT for esophageal luminal defects, including post-surgical anastomotic leaks and transmural perforations (spontaneous or iatrogenic), included 15 single center retrospective cohort studies. A total of 366 patients were included, of which 17.8% were Boerhaave syndrome patients. Clinical success was defined as complete closure of the esophageal defect and was achieved in 87.95% of all patients (95% CI 84.46–91.05%) for all indications. On subgroup analysis it was 88.89% (95% CI 83.22–93.51%) for full-thickness perforations (spontaneous and iatrogenic). The mean duration of treatment was 16.2 days (95% CI 12.6–19.9), with a mean number of 4.6 (95% CI 3.7–5.5) sponge exchanges per patient at a typical interval of 3.7 days (95% CI 3.4–4.1). The attributable mortality of EVT was 4.2% (95% CI 2.3–6.6). Any EVT-related AE was 12.6% (95% CI 10.3–14.7), stricture/dysphagia on follow-up was 5.5% (95% CI 2.1–7.8) and mean sponge migration was 2.6 episodes per patient. 8.5% of patients also received adjunctive SEMS placement in combination with EVT.42 

A 2025 retrospective study was performed to assess the efficacy of EVT in a dedicated cohort of Boerhaave syndrome. The retrospective multicenter German study of 57 patients with Boerhaave syndrome treated their patients with either EVT (25/57), stents (SEMS) (15/57) or surgery (14/57). The authors used standard intraluminal or intracavitary sponge/open pore drains with negative pressure. The median duration of treatment with EVT was 17 days (1-84) with a median cycle of 3 exchanges (0-21). Primary EVT success was achieved in 80% of patients, whereas in the non EVT group success was 43.8% and success for those treated with stents only 26.7%. On multivariable analysis, primary EVT was independently associated with treatment success. EVT failure was documented in 5/25 (20%), two patients died during EVT and three required stents or surgery. In-hospital mortality was 8% with EVT, 14% with surgery, and 33% with stenting. EVT should be concomitantly paired with pleural drainage. Forty-two percent of patients underwent percutaneous drainage or VATS, highlighting the fact that EVT often needs to be performed alongside other very invasive interventions.43

True head-to-head studies comparing the different endoscopic modalities specifically in Boerhaave syndrome are lacking, likely due to the emergent nature of the disorder. The largest comparative data come from a single center retrospective German study on 71 esophageal leaks, which included only three patients with Boerhaave syndrome. They treated their patients with either SEMS or EVT. In this study EVT was preferentially used for larger defects (> 9 mm in size) whereas the stented group had leaks of smaller size. The median duration of therapy was 23 days for the EVT group and 33 days for the stented group. EVT achieved a significantly higher leak closure rate (84.4% vs 53.8%, p < 0.05). Adverse events were higher in the stented group with 28% developing strictures and 15% experiencing stent migration. The EVT group had significantly fewer strictures (9.4%) and a low sponge dislocation rate (2.3%).44 EVT therapy, it should be noted, is very cost and labor intensive requiring multiple procedures per patient in a short period of time, which not all patients can tolerate.

VAC Stents

The main underlying challenge in the management of Boerhaave syndrome is prevention and treatment of mediastinal sepsis. Stents are often effective if placed very soon after the injury occurs and before any appreciable fluid collection has developed. Patients with fluid collections may need drains regardless of what other therapies are applied. Negative-pressure endoscopic therapies provide continuous drainage, healing and allow for endoscopic re-assessment.45 Vacuum-assisted stent systems (VACStent GmbH., Germany) combine the benefits of covered stents and EVT by maintaining luminal patency and encouraging early oral intake. VACStent consists of a fully covered self-expanding nitinol stent (similar size to a standard FCSEMS) with a black open-pore polyurethane foam in the mid-portion of the stent. A thin drainage tube exits proximally from the stent-sponge complex to connect to an external vacuum pump. Continuous negative pressure (-80 to -125 mm Hg) pulls the esophageal wall and leak cavity firmly against the sponge sleeve. The combined mechanism allows sealing of the defect with luminal diversion and continuous drainage of the periesophageal cavity. The negative pressure draws the wall snugly on to the sponge, which helps anchor the device and lowers the risk of migration compared with a standard fully covered stent.46 

A systematic review on 65 patients with 10 Boerhaave syndrome used VAC Stents for treating esophageal and GEJ transmural defects. Most patients needed a total of 1-3 VAC Stents. The mean duration of therapy was 8.8 +-8.3 days (5 to 14 days) and the average interval for changing the VAC Stent was 5.3 days (2-8). Shorter duration and fewer exchanges may improve patient comfort. Clinical success was noted in 50/65 patients (77%). 23% needed additional intervention mostly with further EVT or surgery.47

Similar outcomes were reported in another retrospective case series on the use of VAC Stents in seven patients, of which one had Boerhaave syndrome. The patient required threeVAC Stents, withsuccessful closure after 21 days.48 Although early data suggest VAC Stent is effective, with shorter treatment, fewer exchanges, and earlier oral intake, robust comparative data with standard EVT is still lacking. 

TTS (through-the-scope) Clips and Over the Scope Clips (OTSC)

Clips in the context of Boerhaave syndrome have been used for many years. (Figure 4) They have a clinical efficacy of more than 90% in small (<1–1.5 cm), sharply demarcated perforations with minimal contamination.49 The defects in patients with Boerhaave syndrome are often large with edematous, and may have necrotic ragged edges making them difficult to be approximated by OTSC.

OTSC and TTS have been reported in case series of early contained Boerhaave syndrome or as an adjunct modality.50,51

A case report described how a 2.5 cm Boerhaave syndrome tear was successfully sealed by combining an OTSC with a fully covered self-expanding metal stent. The stent was endoscopically sutured in place to prevent migration. These modalities were combined with aggressive thoracic drainage.52

In a single center series on 14 Boerhaave syndrome patients, 10 were treated primarily with surgery and two with endoscopic therapy and the others with conservative approaches. Overall, 7/14 required SEMS and 3/14 needed OTSC as an adjunct together with thoracic drainage. Primary surgery alone achieved a clinical success rate of 50% whereas endoscopic therapy had 85% clinical success. No patient needed additional surgery and only one death was reported after endoscopy.53

In a case report, a recurrent fibrotic Boerhaave syndrome tear (third transmural rupture) was successfully treated with OTSC and SEMS.54

TTS to treat Boerhaave syndrome has been described only in a handful of case reports. A case series described three patients with contained perforations and these were successfully treated with immediate clipping at presentation. However, the authors advised their use only for short linear defects.55

Conclusion

Outcomes in patients with Boerhaave syndrome are mostly driven by early diagnosis with prompt control of mediastinal sepsis. With the recent advances in therapeutic endoscopy, management has shifted more towards minimally invasive approaches via endoscopy with possible percutaneous catheter drainage, while surgery is needed in only a minority of cases. 

No single approach is ideal for every patient. Combined approaches are often required, especially in patients with complex injuries. Observational cohorts have shown that EVT is an emerging option especially for large, contaminated leaks. It has higher closure rates and fewer strictures compared to conventional stenting alone and can be combined with stents as needed. SEMS and VAC Stent systems permit early oral intake with a shorter treatment course. OTSC and TTS clips are often used in patients with early, well-localized perforations with minimal contamination. 

References

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13. Kochar T, Dhingra PS, Khaliq MF, McJunkin B. Eosinophilic esophagitis presenting with spontaneous esophageal rupture: a case report. J Med Case Rep. 2019;13(1):275.

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15. Çarkıt S, İpekten F, Karaağaç M, Gök M, Akyuz M. Esophageal perforation management: a single-center experience. Ulus Travma Acil Cerrahi Derg. 2024;30(12):875-82.

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19. Shahriarirad R, Karoobi M, Shekouhi R, Ebrahimi K, Ranjbar K, Amirian A, et al. Esophageal perforation etiology, outcome, and the role of surgical management – an 18-year experience of surgical cases in a referral center. BMC Surg. 2023;23(1):177.

20. Kim JD. Prognostic factors of esophageal perforation and rupture leading to mortality: a retrospective study. J Cardiothorac Surg. 2021;16(1):291.

21. Wei CJ, Levenson RB, Lee KS. Diagnostic Utility of CT and Fluoroscopic Esophagography for Suspected Esophageal Perforation in the Emergency Department. AJR Am J Roentgenol. 2020;215(3):631-8.

22. Awais M, Qamar S, Rehman A, Baloch NU, Shafqat G. Accuracy of CT chest without oral contrast for ruling out esophageal perforation using fluoroscopic esophagography as reference standard: a retrospective study. Eur J Trauma Emerg Surg. 2019;45(3):517-25.

23. Suarez-Poveda T, Morales-Uribe CH, Sanabria A, Llano-Sánchez A, Valencia-Delgado AM, Rivera-Velázquez LF, et al. Diagnostic performance of CT esophagography in patients with suspected esophageal rupture. Emerg Radiol. 2014;21(5):505-10.

24. Evans BA, Craig WY, Cinelli CM, Siegel SG. CT esophagogram in the emergency setting: typical findings and suggested workflow. Emerg Radiol. 2024;31(1):33-44.

25. Madsen HJ, Stuart CM, Wojcik BM, Dyas AR, Hunt A, Helmkamp LJ, et al. Esophagram should be performed to diagnose esophageal perforation before inter-hospital transfer. J Thorac Dis. 2023;15(6):2984-96.

26. Zimmermann M, Hoffmann M, Jungbluth T, Bruch HP, Keck T, Schloericke E. Predictors of Morbidity and Mortality in Esophageal Perforation: Retrospective Study of 80 Patients. Scand J Surg. 2017;106(2):126-32.

27. Axtell AL, Gaissert HA, Morse CR, Premkumar A, Schumacher L, Muniappan A, et al. Management and outcomes of esophageal perforation. Dis Esophagus. 2022;35(1).

28. Allaway MGR, Morris PD, JL BS, Richardson AJ, Johnston ES, Hollands MJ. Management of Boerhaave syndrome in Australasia: a retrospective case series and systematic review of the Australasian literature. ANZ J Surg. 2021;91(7-8):1376-84.

29. Haveman JW, Nieuwenhuijs VB, Kobold JP, van Dam GM, Plukker JT, Hofker HS. Adequate debridement and drainage of the mediastinum using open thoracotomy or video-assisted thoracoscopic surgery for Boerhaave’s syndrome. Surg Endosc. 2011;25(8):2492-7.

30. Lee AHH, Kweh BTS, Gillespie C, Johnson MA. Trans-hiatal repair for Oesophageal and Junctional perforation: a case series. BMC Surg. 2020;20(1):41.

31. Cho JS, Kim YD, Kim JW, I HS, Kim MS. Thoracoscopic primary esophageal repair in patients with Boerhaave’s syndrome. Ann Thorac Surg. 2011;91(5):1552-5.

32. Chung MG, Kang DH, Park DK, Park JJ, Park HC, Kim JH. Successful treatment of Boerhaave’s syndrome with endoscopic insertion of a self-expandable metallic stent: report of three cases and a review of the literature. Endoscopy. 2001;33(10):894-7.

33. Margaris I, Triantafyllou T, Sidiropoulos TA, Sideris G, Theodorou D, Arkadopoulos N, et al. Efficacy of esophageal stents as a primary therapeutic option in spontaneous esophageal perforations: a systematic review and meta-analysis of observational studies. Ann Gastroenterol. 2024;37(2):156-71.

34. Anundsen TK, Førland DT, Johannessen HO, Johnson E. Outcome after stent and endoscopic vacuum therapy-based treatment for postemetic esophageal rupture. Scand J Gastroenterol. 2024;59(1):1-6.

35. Kooij CD, Boptsi E, Weusten B, de Vries DR, Ruurda JP, van Hillegersberg R. Treatment of Boerhaave syndrome: experience from a tertiary center. Surg Endosc. 2025;39(4):2228-38.

36. https://www.atsjournals.org/doi/abs/10.1164/ajrccm.2025.211.Abstracts.A6206.

37. Sain S, Panara C, Jena SS, Yadav A, Nundy S. Small bowel obstruction due to migrated oesophageal metal stent. Int J Surg Case Rep. 2025;128:111034.

38. Heits N, Stapel L, Reichert B, Schafmayer C, Schniewind B, Becker T, et al. Endoscopic endoluminal vacuum therapy in esophageal perforation. Ann Thorac Surg. 2014;97(3):1029-35.

39. Loske G, Albers K, Mueller CT. Endoscopic negative pressure therapy (ENPT) of a spontaneous oesophageal rupture (Boerhaave’s syndrome) with peritonitis – a new treatment option. Innov Surg Sci. 2021;6(2):81-6.

40. E410-E411 ES, 10.1055/s-0034-1392597 D.

41. Kim YE, Do YW, Cho JY, Kim ES, Lee DH. Successful Treatment Using Endoluminal Vacuum Therapy after Failure of Primary Closure in Boerhaave Syndrome. Korean J Gastroenterol. 2019;73(4):219-24.

42. Vohra I, Gopakumar H, Sharma NR, Puli SR. Efficacy of endoscopic vacuum therapy in esophageal luminal defects: a systematic review and meta-analysis. Clin Endosc. 2025;58(1):53-62.

43. Wannhoff A, Kouladouros K, Koschny R, Walter B, Zoll Z, Büringer K, et al. Endoscopic vacuum therapy for the treatment of Boerhaave syndrome: a multicenter analysis. Gastrointest Endosc. 2025;101(2):365-74.

44. Brangewitz M, Voigtländer T, Helfritz FA, Lankisch TO, Winkler M, Klempnauer J, et al. Endoscopic closure of esophageal intrathoracic leaks: stent versus endoscopic vacuum-assisted closure, a retrospective analysis. Endoscopy. 2013;45(6):433-8.

45. Saqib M, Iftikhar M, Ahmed K, Shahid H, Shehr I, Khan Y, et al. Esophageal stenting and endoscopic vacuum therapy for esophageal defects: a systematic review and meta-analysis of observational studies. Ann Med Surg (Lond). 2025;87(9):5963-72.

46. Klose MA, Walldorf J, Damm M, Krug S, Klose J, Ronellenfitsch U, et al. Treatment of esophageal leakages with the Microtech(®)-VAC-Stent: a monocentric early experience of three cases. Ther Adv Gastrointest Endosc. 2023;16:26317745231200312.

47. Kehagias D, Abogabal S, Lampropoulos C, Haider MI, Kehagias I, Jain P, et al. VacStent as a novel therapeutic approach for esophageal perforations and anastomotic leaks- a systematic review of the literature. BMC Surg. 2025;25(1):309.

48. González Aldama M, Santa Cruz Carrera M, López García ML, Prado Troya NF, Irusta Olano L, Jiménez Pérez MA, et al. VACStent therapy for treatment of esophageal transmural defects: early experience in a tertiary hospital. Endoscopy. 2025;57(S 02):eP440.

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51. Kobara H, Mori H, Rafiq K, Fujihara S, Nishiyama N, Kato K, et al. Successful endoscopic treatment of Boerhaave syndrome using an over-the-scope clip. Endoscopy. 2014;46 Suppl 1 UCTN:E82-3.

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55. Otsuka K, Murakami M, Ariyoshi T, Yamashita T, Goto S, Watanabe M, et al. Endoscopic clipping of spontaneous esophageal rupture: Case reports of three patients. Int J Surg Case Rep. 2017;38:18-22.

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Dispatches from the GUILD Conference, Series #72

Computer-Aided Detection in Colonoscopy: Promise, Performance, and Real-World Questions

February 2026 • Volume MMXXVI, Issue 2
Tasnim Ahmed,Stephen Le Breton,Tyler M. Berzin

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Computer aided polyp detection (CADe) is one of the most heavily studied applications of artificial intelligence in clinical medicine and may serve as a valuable adjunct for gastrointestinal endoscopists. Randomized controlled trials have demonstrated that CADe improves adenoma detection rates, particularly of smaller polyps and sessile serrated lesions. In this review, we provide an overview of the potential benefits and harms associated with CADe, as well as the limitations observed in real-world implementation. While modeling studies have demonstrated that CADe may be a cost-effective strategy to improve colonoscopy quality, it remains to be seen whether it will have a meaningful impact on colon cancer incidence rates, highlighting an important direction for future research. 

Introduction

Colorectal cancer prevention through screening colonoscopy depends on one critical factor: the reliable detection and removal of precancerous polyps. Recent society guidelines increased the adenoma detection rate (ADR) performance goal from 25% to 35%, with differing thresholds by sex.1 While numerous tools and techniques have been introduced over the years to enhance polyp detection, few have yielded performance gains as substantial as those seen with the advent of computer-aided polyp detection (CADe).2 As missed lesions are a major driver of post-colonoscopy colorectal cancer (PCCRC), CADe may offer a meaningful opportunity to reduce this risk.3 (Fig 1a./1b.). Although more than 40 randomized trials have demonstrated the benefit of CADe in increasing polyp detection, real-world data have been more variable.4 Important questions remain about the clinical benefit and cost-effectiveness of CADe across varied clinical settings, and whether incremental gains in ADR can further reduce colon cancer risk, particularly among endoscopists who already meet or exceed established quality benchmarks.5

The State of Evidence for CADe

The evidence demonstrating the benefit of CADe-assisted colonoscopies is generally very strong with numerous trials across North America, Europe, and China demonstrating that CADe improves polyp and adenoma detection rates, which are important surrogate markers for long term outcomes linked to preventing colorectal cancer incidence. Early clinical trials that compared standard colonoscopy to colonoscopies with computer-aided detection found a significant increase in ADR when artificial intelligence systems were used.6 Wang et al.’s study, which was one of the first to investigate CADe, found that AI-assistance significantly increased ADR from 20% to 29%. Wallace et al. later investigated the impact of AI on adenoma miss rates, or the number of lesions that were missed by an initial colonoscopy, calculated as a ratio of adenomas detected in a second colonoscopy to the cumulative detected between the first and second. This study found that AI detection tools reduced the miss rate of neoplasia two-fold, improving the efficacy of screening colonoscopies.7

Much of the documented benefit of CADe technology seems to be driven by improving detection of smaller polyps. Hassan et al. conducted a meta-analysis of 21 randomized control trials investigating CADe and found that overall, CADe did not increase the number of advanced adenomas identified per patient, but did increase the number of diminutive adenomas, or adenomas that are less than 5mm, identified per colonoscopy.8 Another meta-analysis involving 25 trials found that CADe was associated with higher sessile serrated lesion detection rates (SSLDR).9 These are the same lesions that are often missed and responsible for post-colonoscopy colorectal cancers, or cancers that are diagnosed after an initial negative colonoscopy.10 Considering the updated quality benchmarks for colonoscopy in 2024 now call for SSLDR as a new priority quality indicator, emerging data regarding the ability of CADe to improve sessile lesions is particularly important.1

Variable Impact of AI

The effects of CADe on polyp detection also seem to vary in different clinical settings and in the hands of different endoscopists. For instance, in several community-based and observational trials, CADe benefit has been more variable.11 In fact, one study even showed that CADe seemed to have a negative effect, leading to lower ADR after it was introduced in a large volume center to assess its real-world capabilities.12 There are a variety of potential explanations for this, ranging from variability in baseline adenoma detection rates, endoscopist engagement with the technology, to subtle differences in clinical practice environments—all of which may influence real-world effectiveness of technology adoption. These findings underscore that while CADe offers promise, its performance is not immune to clinical context and operator factors. 

Another factor that may influence the benefit of CADe is the expertise and baseline performance level of the endoscopist performing the procedure. Studies conducted in settings with lower average ADRs have shown that CADe can significantly enhance detection, helping to close quality gaps.8 Among those with already high ADR, the added benefit of CADe appears more limited, suggesting a ceiling effect where the opportunity for further improvement is inherently constrained. Moreover, even if CADe does provide an ADR benefit for physicians with high baseline ADR, it is questionable whether these incremental performance gains translate to real clinical benefit for patients by reducing interval colon cancer risk.5 

The observation that AI appears to disproportionately benefit less experienced endoscopists has also sparked ongoing debate around its impact on innate skill.13 A retrospective study from Poland evaluated adenoma detection rates in endoscopists three months before and after implementation of CADe in their endoscopy suites. Interestingly, the study found a small decline in ADR when endoscopists returned to conventional colonoscopy, raising concerns that prolonged reliance on CADe might degrade natural detection ability, otherwise known as “de-skilling”.14 However, on closer analysis, it seems unlikely that this represents true erosion of skill as it’s difficult to imagine that well-established pattern recognition and polyp detection instincts would disappear after only a few months of AI use. More plausibly, this reflects a natural cognitive adaptation, a shift in attention or off-loading of certain detection tasks to the AI. As with pilots using autopilot, some redistribution of cognitive effort is expected when humans operate alongside assistive technologies. This attentional rebalancing may reduce vigilance in the short term but does not necessarily imply permanent loss of ability. 

Moreover, this type of cognitive adaptation is neither surprising nor unique to medicine. It mirrors what we observe across many domains of life with the steady march of technology. Just as drivers recalibrate their spatial awareness when using GPS, or pilots adjust attentional focus when flying with autopilot, endoscopists working alongside CADe to naturally redistribute cognitive effort. These shifts don’t necessarily signal loss of skill but rather an evolution in how expertise is applied when augmented by technology. Nonetheless, it will be critical to design clinical training and workflow models that preserve core clinical capabilities while leveraging the advantages of AI.

It’s certainly possible that with diligence, AI can be safely incorporated into screening colonoscopy, without decreasing endoscopists’ skill level, as many individual endoscopist had demonstrated in this study. However, what is less certain is the impact that AI may have on trainees who have yet to build a foundational skillset. “Never-skilling” is the concept that a novice or trainee never manages to develop the core competencies for endoscopy because they are likely to rely heavily on computer vision to identify abnormal polyps versus their own intuition. It is undeniable that CADe improves the quality of trainees’ colonoscopies by significantly increasing ADR and SSLDR and helps to meet benchmarks delineated by the American College of Gastroenterology.15 Combatting “never-skilling” may look like implementing accreditation requirements that trainees complete some number of colonoscopies without AI-assistance to become competent on their own. 

Slow Adoption from Societies

There continues to be hesitancy in the large-scale adoption of CADe. Early last year, the British Medical Journal released a living practice guideline that recommended against the routine use of CADe in adults undergoing a colonoscopy.16 Much of this is due to inconclusive and variable data on whether CADe significantly improves adenoma detection rate to lead to an actual reduction in colon cancer prevalence. Given the relative infancy of artificial intelligence tools, there are no longitudinal studies yet to assess the long-term impact of CADe on reducing colorectal cancer rates. A microsimulation study was conducted to model the impact of CADe on 10-year colorectal cancer incidence and mortality rates amongst patients aged 60 to 69. The study concluded that there would be no significant change in colorectal cancer incidence with CADe.17 However, the study is unable to account for the constantly evolving nature of these artificial intelligence tools, which stands to improve in effectiveness over time. 

Society guidelines also acknowledge the risks associated with widespread incorporation of CADe. The same modeling study found that while there were no significant differences in adverse events for either arm, CADe could lead to increased unnecessary surveillance after screening colonoscopies and a higher burden on the health care system.17 CADe may also lead to unnecessary resections, mostly of small hyperplastic polyps. Altogether, these additional interventions would culminate in additional and unnecessary healthcare spending and brings to question the cost-effectiveness of this tool.

Cost Effectiveness of CADe

Currently, there are only a few CADe devices that have FDA approval, and their widespread implementation would come with an initial upfront cost. However, over time, the hope is that money saved from avoiding costly colorectal cancer treatment would offset this investment. One group of researchers modeled the economic implications of artificial intelligence on screening colonoscopies for the US health care system. They estimated that the costs of AI systems would be $19 per procedure based on the prices of available AI tools at the time of the study.18 The marginal benefit of AI colonoscopy on colorectal cancer incidence and mortality had a significant impact on overall cost to the health care system. The model showed that screening colonoscopies with AI would reduce the cost of a colonoscopy by $57 per individual when assuming just a 60% screening uptake, even when accounting for additional surveillance colonoscopies and polypectomies with pathology. Yearly, this would amount to $290 million of savings for the country.18 So, while AI-assisted colonoscopies may lead to more surveillance, in the long term it may still be cost effective on a population level.

Beyond CADe: CADx, CAQ and More

Following computer aided detection, the natural next step in implementing artificial intelligence to streamline colorectal cancer screening would be to use AI to aid in polyp diagnosis. Computer-aided diagnosis (CADx) enables endoscopists the ability to visually distinguish between non-neoplastic and neoplastic polyps without pathological review. Currently, many endoscopists conservatively elect to resect all polyps, given the difficulty in discriminating between polyps that will develop into cancer and those that will not, resulting in unnecessary resections of non-neoplastic polyps. 

CADx tools assist optical diagnosis by providing a real-time prediction to the endoscopist, regarding whether a polyp is adenomatous or hyperplastic. For ruling out neoplastic lesions (precancerous polyps), CADx algorithms demonstrated a high negative predictive value of greater than 90% in an early study.19 However, across numerous clinical trials, it remains unclear whether CADx can meaningfully impact clinical practice for instance by supporting a ‘resect and discard’ strategy for small polyps.20 Like CADe, studies that evaluated real-time use of CADx have demonstrated that its efficacy may vary by endoscopist experience and polyp morphology.21 Looking ahead, as the technology continues to advance and improve, CADx might also be a promising technology to explore in low-resourced settings, where pathologists and labs are scarce.

Recently, the FDA has also approved a computer-aided quality assessment (CAQ) tool that can serve to measure colonoscopy quality by incorporating factors such as bowel preparation, withdrawal time, and cecal intubation. Pilot studies show promise that the technology is making progress towards measuring certain colonoscopy quality indicators (e.g., cecal landmarks and withdrawal time), although alignment between endoscopist bowel prep scoring and AI bowel prep scoring remains a challenge.22

Conclusion

AI-assisted colonoscopy is among the most extensively studied applications of artificial intelligence in clinical medicine, with growing evidence and rising enthusiasm pointing toward its inevitable integration into routine practice.23 But gastroenterologists must be vigilant of how heavily they rely on these tools as an adjunct to their own clinical acumen. Different gastrointestinal societies have been hesitant to embrace these tools in their recommendations due to an uncertainty over the real-world effects on downstream colon cancer risk. Some of the heterogeneity in published outcomes may be explained by variability in endoscopists’ baseline expertise, technique, and adenoma detection performance. In general, endoscopists with less experience or lower baseline adenoma detection rates appear more likely to derive measurable benefit from AI assistance, but this also raises legitimate concerns about “deskilling” and “never skilling,” particularly in trainees. However, these AI tools appear to provide a tangible mechanism to improve the quality of colonoscopies and modeling studies hint that improvements in colonoscopy quality associated with AI assistance could ultimately yield downstream healthcare cost savings. AI assistance for adenoma detection is still in an early phase of the adoption curve, and as models continue to be trained, their efficacy too will likely improve. With a healthy degree of caution, implementing these tools can help gastroenterologists meet important benchmarks and improve clinical care. 

References

1. Rex DK, Anderson JC, Butterly LF, et al. Quality Indicators for Colonoscopy. Official journal of the American College of Gastroenterology | ACG 2024;119(9):1754-80. doi: 10.14309/ajg.0000000000002972

2. Aziz M, Haghbin H, Sayeh W, et al. Comparison of Artificial Intelligence With Other Interventions to Improve Adenoma Detection Rate for Colonoscopy: A Network Meta-analysis. J Clin Gastroenterol 2024;58(2):143-55. doi: 10.1097/mcg.0000000000001813 [published Online First: 2022/11/29]

3. Pohl H, Robertson DJ. Colorectal Cancers Detected After Colonoscopy Frequently Result From Missed Lesions. Clinical Gastroenterology and Hepatology 2010;8(10):858-64. doi: 10.1016/j.cgh.2010.06.028

4. Patel HK, Mori Y, Hassan C, et al. Lack of Effectiveness of Computer Aided Detection for Colorectal Neoplasia: A Systematic Review and Meta-Analysis of Nonrandomized Studies. Clinical Gastroenterology and Hepatology 2024;22(5):971-80.e15. doi: 10.1016/j.cgh.2023.11.029

5. Pilonis ND, Spychalski P, Kalager M, et al. Adenoma Detection Rates by Physicians and Subsequent Colorectal Cancer Risk. Jama 2025;333(5):400-07. doi: 10.1001/jama.2024.22975 [published Online First: 2024/12/16]

6. Wang P, Berzin TM, Glissen Brown JR, et al. Real-time automatic detection system increases colonoscopic polyp and adenoma detection rates: a prospective randomised controlled study. Gut 2019;68(10):1813-19. doi: 10.1136/gutjnl-2018-317500 [published Online First: 2019/03/01]

7. Wallace MB, Sharma P, Bhandari P, et al. Impact of Artificial Intelligence on Miss Rate of Colorectal Neoplasia. Gastroenterology 2022;163(1):295-304.e5. doi: https://doi.org/10.1053/j.gastro.2022.03.007

8. Hassan C, Spadaccini M, Mori Y, et al. Real-Time Computer-Aided Detection of Colorectal Neoplasia During Colonoscopy. Annals of Internal Medicine 2023;176(9):1209-20. doi: 10.7326/M22-3678

9. Ahmed T, Ali FS, Hicklen R, et al. S1246 e-Examining Computer-Aided Polyp Detection in the Era of a New Quality Benchmark: A Meta-Analysis of ADR, PDR, and SSLDR. Official journal of the American College of Gastroenterology | ACG 2025;120(10S2):S269. doi: 10.14309/01.ajg.0001132444.28699.b5

10. Troelsen FS, Sørensen HT, Pedersen L, et al. Root-cause Analysis of 762 Danish Post-colonoscopy Colorectal Cancer Patients. Clin Gastroenterol Hepatol 2023;21(12):3160-69.e5. doi: 10.1016/j.cgh.2023.03.034 [published Online First: 2023/04/10]

11. Wei MT, Shankar U, Parvin R, et al. Evaluation of Computer-Aided Detection During Colonoscopy in the Community (AI-SEE): A Multicenter Randomized Clinical Trial. Official journal of the American College of Gastroenterology | ACG 2023;118(10)

12. Levy I, Bruckmayer L, Klang E, et al. Artificial Intelligence-Aided Colonoscopy Does Not Increase Adenoma Detection Rate in Routine Clinical Practice. Am J Gastroenterol 2022;117(11):1871-73. doi: 10.14309/ajg.0000000000001970 [published Online First: 2022/08/25]

13. Lou S, Du F, Song W, et al. Artificial intelligence for colorectal neoplasia detection during colonoscopy: a systematic review and meta-analysis of randomized clinical trials. eClinicalMedicine 2023;66 doi: 10.1016/j.eclinm.2023.102341

14. Budzyń K, Romańczyk M, Kitala D, et al. Endoscopist deskilling risk after exposure to artificial intelligence in colonoscopy: a multicentre, observational study. The Lancet Gastroenterology & Hepatology 2025;10(10):896-903. doi: 10.1016/S2468-1253(25)00133-5

15. Orzeszko Z, Gach T, Necka S, et al. The implementation of computer-aided detection in an initial endoscopy training improves the quality measures of trainees’ future colonoscopies: a retrospective cohort study. Surg Endosc 2025;39(8):5276-86. doi: 10.1007/s00464-025-11890-3 [published Online First: 2025/07/01]

16. Foroutan F, Vandvik PO, Helsingen LM, et al. Computer aided detection and diagnosis of polyps in adult patients undergoing colonoscopy: a living clinical practice guideline. BMJ 2025;388:e082656. doi: 10.1136/bmj-2024-082656

17. Halvorsen N, Hassan C, Correale L, et al. Benefits, burden, and harms of computer aided polyp detection with artificial intelligence in colorectal cancer screening: microsimulation modelling study. BMJ Med 2025;4(1):e001446. doi: 10.1136/bmjmed-2025-001446 [published Online First: 2025/04/01]

18. Areia M, Mori Y, Correale L, et al. Cost-effectiveness of artificial intelligence for screening colonoscopy: a modelling study. The Lancet Digital Health 2022;4(6):e436-e44. doi: 10.1016/S2589-7500(22)00042-5

19. Kominami Y, Yoshida S, Tanaka S, et al. Computer-aided diagnosis of colorectal polyp histology by using a real-time image recognition system and narrow-band imaging magnifying colonoscopy. Gastrointestinal Endoscopy 2016;83(3):643-49. doi: https://doi.org/10.1016/j.gie.2015.08.004

20. Hassan C, Rizkala T, Mori Y, et al. Computer-aided diagnosis for the resect-and-discard strategy for colorectal polyps: a systematic review and meta-analysis. The Lancet Gastroenterology & Hepatology 2024;9(11):1010-19. doi: https://doi.org/10.1016/S2468-1253(24)00222-X

21. Bustamante-Balén M. Role of CADx in colonoscopy: lessons from real-life studies. Best Practice & Research Clinical Gastroenterology 2025:102020. doi: https://doi.org/10.1016/j.bpg.2025.102020

22. Brenner TA, Labaki C, Feuerstein JD, et al. Prospective Validation of the First US FDA-Approved Computer-Aided Quality Assessment Tool for Colonoscopy: An Initial Clinical Experience. The American journal of gastroenterology 2025 doi: 10.14309/ajg.0000000000003855

23. Han R, Acosta JN, Shakeri Z, et al. Randomised controlled trials evaluating artificial intelligence in clinical practice: a scoping review. Lancet Digit Health 2024;6(5):e367-e73. doi: 10.1016/s2589-7500(24)00047-5 [published Online First: 2024/04/27]

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INTRODUCTION: DISPATCHES FROM THE GUILD CONFERENCE

Introduction: Dispatches from the 10th Annual GUILD Conference 2026

February 2026 • Volume MMXXVI, Issue 2
Uma Mahadevan

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Welcome to the tenth 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 2026: February 15 -18) and a new meeting in the Caribbean, this year in Puerto Rico, in January 2026. We are delighted to offer a hybrid meeting in Maui with over 275 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, irritable bowel syndrome, artificial intelligence and colon cancer. 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 Caribbean meeting.

To share our learning with the gastroenterology community at large, we are happy to continue our series beginning with the following article, “Computer-Aided Detection in Colonoscopy:Promise, Performance, and Real-World Questions”.

We look forward to providing informative and educational articles covering IBD, Hepatology, and general gastroenterology in Practical Gastroenterology over the following months. We hope to see you all in person for GUILD 2027 in Puerto Rico (January 17-20, 2027) and in Maui (February 14 -17, 2027). 

For more information on the
GUILD Conference, visit:

guildconference. com

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Fellows’ Corner

February 2026 • Volume MMXXVI, Issue 2

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by Archit Garg

The patient, a 46-year-old woman, came to the emergency room with three blisters on her right leg, which had appeared a week prior and were getting bigger. No recent trauma, bites, or contact with seawater were noted. Never before had she encountered such lesions.

Previous medical issues: ulcerative colitis (diagnosed eight years ago), type 2 diabetes, and recurring iliopsoas abscesses due to uncontrolled diabetes, which needed several surgical drainages. She currently takes insulin, mirikizumab, mesalamine enemas, and budesonide, but she stopped taking budesonide two weeks ago.

On presentation, she was febrile (103°F) and tachycardic (HR 104 bpm). The physical examination is illustrated in Figure 1. There was no soft tissue gas detected on the lower extremity CT scan. During hospitalization, the bullae ruptured, leaving ulcers (Figure 2). Cultures taken from the ulcer remain negative. A biopsy was performed, which is shown in Figure 3.

Question 1: 

Which of the following is the treatment choice for the above condition?

A) High-dose systemic corticosteroids 

B) Broad-spectrum intravenous antibiotics

C) Surgical debridement and drainage

D) Intensive insulin therapy and glycemic control

E) Total colectomy

Correct Answer: A 

Explanation

Pyoderma gangrenosum (PG) is the condition described above. The patient has a history of ulcerative colitis and painful purple blisters (Figure 1) that turned into ulcers (Figure 2), with purple, eroded edges, a dead base, and surrounding redness. The biopsy of the skin lesion shows an abundant neutrophilic infiltrate with leukocytoclasia and necrosis, strongly suggesting PG (Figure 3).

The first-line treatment for acute, severe PG is corticosteroids. Corticosteroids are potent anti-inflammatory and immunosuppressive agents that cause the sequestration of CD4+ T-lymphocytes and inhibit the transcription of cytokines. The usual dose is 0.5-1.5mg/kg per day of oral prednisone or its equivalent. Pulse therapy with 1 g methylprednisolone for 1-5 days may be considered for aggressive disease. The patient’s recent cessation of budesonide may have contributed to this flare, making re-initiation of a high-dose steroid imperative.  The response to steroids is usually rapid, and studies have shown complete healing after 6 months in about half of the patients.1,2

Option B:

While the ulcer may appear infected, in a setting of febrile presentation with immunosuppression, antibiotics are often initiated. However, the negative cultures, lack of evidence of primary infection (no gas on CT scan and bacteremia) indicate an autoimmune process, and antibiotics are ineffective in treating PG.

Option C:

Surgical debridement is contraindicated in the management of PG. In fact, surgery can provoke pathergy (trauma to the skin causing new, large ulcer formation). Debridement should be absolutely avoided in the initial phase of presentation.3 In rare circumstances, once active disease is controlled and the ulcers are in the healing phase, careful removal of dead necrotic tissue can be considered. 

Option D: 

Optimizing glycemic control is essential for the supportive management of diabetic patients. Echthyma gangrenosum is a pseudomonal skin infection that typically manifests in individuals with uncontrolled diabetes. However, the absence of a typical clinical presentation (hemorrhagic bulla or pustule followed by necrotic ulcer) and bacteremia rules out ecthyma gangrenosum.

Option E:

Total colectomy was once considered a treatment option for PG, specifically in the context of peristomal PG associated with active IBD.4 However, current recommendations are medical immunosuppression, given the significant morbidity and mortality associated with surgical interventions. 

Question 2: What is the pathogenesis of pyoderma gangrenosum?

PG is classified as a neutrophilic dermatosis. It arises from a complex dysregulation of innate and adaptive immunity. It involves dysregulated immune responses, with neutrophil recruitment and activation mediated by cytokines such as IL-1β, TNF-α, and IL-17. [5] Th17/Th1 skewing and a neutrophil-driven inflammatory cascade marked by elevated cytokines (e.g., TNF-α, IL-1β, IL-17, IL-23, IL-36) are caused by antigenic priming in genetically predisposed individuals. IL-1β release is further amplified by genetic variants that impact the inflammasome pathways (PSTPIP1, MEFV, NLRP3, NLRP12, and NOD2). In addition to complement (C5a), NETosis, T-cell imbalance, and other triggers, such as trauma (pathergy), cause keratinocytes to release cytokines that contribute to the pathogenesis.6

Question 3: What is the prognosis of pyoderma gangrenosum?

Nearly 50% of patients who receive treatment for PG achieve complete wound healing within one year. New lesions can develop during or after healing of other lesions, and relapses can occur after the disease has remained quiescent for months to years. The triggers for relapse can be minimal trauma, surgery, or, in some cases, no apparent trauma. PG is a lethal disease with reported mortality as high as 30%. Male sex, old age of onset, and bullous PG in the presence of hematological malignancies or disorders are some poor prognostic factors.6 Death may occur due to underlying associated disorders (e.g., malignancy), sepsis from superimposed infection from the ulcers themselves, or from immunosuppressive therapy. The overall prognosis of pyoderma gangrenosum without underlying disease is good, particularly in those patients who readily respond to treatment, but considerable scarring and disfigurement may eventually result. The overall prognosis for PG in patients without underlying conditions is generally favorable, especially among those who exhibit a prompt response to treatment. However, significant scarring and disfigurement may ultimately occur.7

Question 4: How do immunomodulators compare to corticosteroids in the treatment approach for pyoderma gangrenosum?

The first-line treatment choice for PG remains corticosteroids. This is because of their rapid onset of action in controlling acute inflammation. However, long-term use of steroids is limited due to associated adverse effects. Steroid-sparing agents like immunomodulators, including cyclosporine, tacrolimus, mycophenolate mofetil, azathioprine, and biologics such as anti-TNF agents (e.g., infliximab, adalimumab) or IL-12/23 inhibitors (e.g., ustekinumab), play a crucial role as steroid-sparing agents and as primary therapy in severe, refractory cases. Biologics are often initiated along with steroids in patients with underlying autoimmune conditions associated with PG, for example, IBD, rheumatoid arthritis, etc. Hence, while steroids/cyclosporine remain the initial treatment of choice for rapid control, immunomodulators are essential for long-term disease management, relapse prevention, and minimizing steroid-related toxicity.6,8,9

Question 5: Is pyoderma gangrenosum specific to ulcerative colitis?

No, PG is not specific to ulcerative colitis. Although PG is recognized as a well-known extraintestinal manifestation of IBD (both Crohn’s disease and ulcerative colitis), it can occur independently of IBD. It is associated with rheumatoid arthritis, seronegative arthritis, hematologic disorders (such as leukemia, monoclonal gammopathy, myelodysplastic syndromes), and other autoimmune disorders.10 Moreover, in up to one-third of the cases, the cause of PG is unidentifiable without any associated systemic disease.10

Conclusion

Pyoderma gangrenosum is a severe inflammatory skin condition strongly associated with ulcerative colitis. The first-line treatment is high-dose corticosteroids or cyclosporine. In severe cases, biologic therapy/ immunomodulators, such as infliximab, adalimumab, or mycophenolate, may be added. Surgical intervention is contraindicated due to the risk of worsening skin lesions through pathergy. The entity was first described by Brocq and Simon in 1908 as “phagédénisme géométrique” and subsequently renamed by Brunsting et al. in 1930. (5)  

References

1. Dissemond J, Marzano AV, Hampton PJ, Ortega-Loayza AG.
Pyoderma gangrenosum: treatment options. Drugs. 2023
Sep;83(14):1255-67.
2. Ormerod AD, Thomas KS, Craig FE, Mitchell E, Greenlaw N,
Norrie J, Mason JM, Walton S, Johnston GA, Williams HC.
Comparison of the two most commonly used treatments for
pyoderma gangrenosum: results of the STOP GAP randomised
controlled trial. bmj. 2015 Jun 12;350.
3. Bar D, Beberashvili I. Assessing the role of wound debridement
in pyoderma gangrenosum—A retrospective cohort study.
Wound Repair and Regeneration. 2024 Nov;32(6):941-8.
4. Afifi L, Sanchez IM, Wallace MM, Braswell SF, Ortega-Loayza
AG, Shinkai K. Diagnosis and management of peristomal
pyoderma gangrenosum: a systematic review. Journal of the
American Academy of Dermatology. 2018 Jun 1;78(6):1195-
204.
5. Maronese CA, Pimentel MA, Li MM, Genovese G, Ortega-
Loayza AG, Marzano AV. Pyoderma gangrenosum: an updated
literature review on established and emerging pharmacological
treatments. American journal of clinical dermatology. 2022
Sep;23(5):615-34.
6. Conrad C, Trüeb RM. Pyoderma gangrenosum: Pyoderma gangraenosum.
JDDG: Journal der Deutschen Dermatologischen
Gesellschaft. 2005 May;3(5):334-42.
7. Wolff K. Pyoderma gangrenosum. Dermatology in general
medicine. 1999.
8. Dissemond J, Marzano AV, Hampton PJ, Ortega-Loayza AG.
Pyoderma gangrenosum: treatment options. Drugs. 2023
Sep;83(14):1255-67.
9. Rogler G, Singh A, Kavanaugh A, Rubin DT. Extraintestinal
manifestations of inflammatory bowel disease: current concepts,
treatment, and implications for disease management.
Gastroenterology. 2021 Oct 1;161(4):1118-32.
10. Fischer AH, Jourabchi N, Khalifian S, Lazarus GS. Spectrum of
diseases associated with pyoderma gangrenosum and correlation
with effectiveness of therapy: New insights on the diagnosis
and therapy of comorbid hidradenitis suppurativa. Wound
Repair and Regeneration. 2022 May;30(3):338-44.

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A Case Report

Chalk Pica Presenting as Hypercalcemia-Induced Pancreatitis

February 2026 • Volume MMXXVI, Issue 2

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by Bhaavya Pinnala, Sindhu Naresh, Saleha Asghar

Acute pancreatitis is most commonly associated with gallstone disease, chronic alcohol use or hypertriglyceridemia while metabolic abnormalities such as hypercalcemia are far less frequent.1 Hypercalcemia accounts for only about 1% of acute pancreatitis cases, making it a cause that is not typically encountered in routine clinical practice.1 Among the causes of hypercalcemia-induced pancreatitis (HIP), primary hyperparathyroidism is the most common and accounts for approximately 90% of all hypercalcemia cases.3 

Other causes of hypercalcemia include malignancy, particularly lung cancer, breast cancer, and multiple myeloma, granulomatous diseases (tuberculosis and sarcoidosis), vitamin A or D toxicity, hypothyroidism and medications like thiazide diuretics, lithium, and antacids.2,3

An under-recognized cause of hypercalcemia is chalk ingestion, which often occurs in the setting of pica. Chalk is primarily composed of calcium carbonate and can become a substantial calcium source for individuals who consume it regularly.5 This behavior can raise serum calcium to harmful levels, leading to metabolic disturbances and in this case, hypercalcemia-induced pancreatitis.

Case Presentation

A 52-year-old African American female with past medical conditions of hypothyroidism and newly diagnosed insulin-dependent type 2 diabetes mellitus, presented to the emergency department after a witnessed fall and several days of worsening fatigue and confusion. According to her family, she had been complaining of abdominal pain over the past two days. Additionally, the patient had been experiencing increased urinary frequency.

Her exam was notable for pale appearance and disorientation. The remainder of the physical examination was notable for diffuse abdominal tenderness with guarding. Her vital signs included a blood pressure of 90/60 mmHg, heart rate of 120 beats-per-minute, afebrile and oxygen saturation of 97% on room air. 

Initial laboratory evaluation revealed serum calcium was markedly elevated at 25.4 mg/dL with an ionized calcium of 2.48 mmol/L. Additional findings included an albumin of 3.9 g/dL and an elevated lactate of 3.2 mmol/L. Her lipase was markedly elevated at 1,739U/L. Her liver enzymes, lipid panel and ethanol level were in normal range.

Computed tomography (CT) imaging of the abdomen and pelvis with contrast demonstrated acute interstitial pancreatitis without gallstones or biliary dilation [Imaging 1 & 2]. Additionally, large heterogeneous pelvic mass, suggestive of a uterine leiomyoma, was noted.

She was admitted to the intensive care unit for management of hypercalcemic crisis. The patient received empiric antibiotics, intravenous fluids and underwent two sessions of emergent hemodialysis. Patient’s hypercalcemia improved with hemodialysis and intravenous fluid, without the need for bisphosphonates, or calcitonin. Her calcium levels normalized from 25.4 to 9.4 mg/dL, accompanied by a gradual recovery in mental status. Serum calcium levels normalized within approximately 48 hours of initiating treatment. The patient’s pancreatitis gradually improved as she was able to tolerate oral intake. 

A comprehensive metabolic evaluation demonstrated a suppressed PTH level (5.9 pg/mL) while phosphate, PTHrP, 25-hydroxy vitamin D, and 1,25-dihydroxy vitamin D were within normal limits. Serum and urine electrophoresis, serum free light chains, TSH, lithium, vitamin A level, and urine calcium were all unremarkable. Hematologic studies revealed microcytic anemia with hemoglobin level of 9 g/dl, MCV of 63 fL, low iron (8 µg/dL), a TIBC of 281 µg/dL, ferritin of 37.2 ng/mL, a reticulocyte count of 1.5%, and a peripheral smear showing microcytic, hypochromic red blood cells. 

After resolution of her symptoms, the patient denied the use of diuretics, lithium, antacids, vitamin and calcium supplements. Her workup revealed no identifiable cause of hypercalcemia, raising concern about the source of her severe calcium elevation. It was only later in her hospitalization, when we specifically asked about her dietary habits, that she disclosed regularly consuming powdered chalk for almost three months. She consumed two bags of chalk (approximately four kilograms per day). She had not previously disclosed this due to embarrassment and a belief that the behavior was harmless to her health.

She received intravenous iron and was discharged on oral iron supplementation. She was evaluated by gynecology, and the uterine leiomyoma was removed. At an outpatient follow-up six weeks later, serum calcium (8.9 mg/dl) and hematologic studies returned to normal, and her chalk-ingestion behavior fully resolved. 

Discussion

Hypercalcemia is an uncommon but recognized trigger of acute pancreatitis, accounting for approximately 1–2% of cases. Most HIP are attributed to primary hyperparathyroidism or malignancy-associated hypercalcemia.1 Literature on exogenous calcium leading to pancreatitis is extremely limited, with chalk ingestion described only in isolated cases. Hypercalcemia can precipitate pancreatitis by increasing intracellular calcium levels within pancreatic acinar cells, triggering premature trypsinogen activation and leads to autodigestion and inflammation.2 

HIP is infrequently encountered, but hospitalist and gastroenterology management is pivotal for acute care and recurrence prevention. Priorities include confirming pancreatitis, excluding common pancreatitis etiologies, initiating lactated ringer’s-based resuscitation with adequate analgesia, and starting early enteral nutrition; contrast-enhanced CT is reserved for diagnostic uncertainty or lack of improvement after 48–72 hours, and ERCP is performed only for biliary indications. Close monitoring of electrolytes, with recognition that fat saponification can lead to secondary hypocalcemia as inflammation evolves. Preventing another episode requires addressing the underlying cause of hypercalcemia through a multidisciplinary approach, while counseling patients to avoid hidden or non-nutritive calcium sources. 

Pica is often underreported and maybe normalized by patients who have engaged in the behavior for years. Although geophagia is a recognized form of pica in the DSM-5, psychiatric consultation was not obtained during this hospitalization. An additional consideration, in Central Georgia, kaolin (a form of chalk) is sometimes consumed as part of a cultural practice, particularly among African American women.6 However, both the patient and her family denied any cultural or personal use of kaolin or similar substances.

The current diagnostic algorithm for hypercalcemia begins by confirming elevated calcium levels and reviewing medications and supplements, including thiazide diuretics, lithium, vitamin D, vitamin A, calcium-containing antacids, and other over-the-counter products. Once hypercalcemia is established, intact PTH is measured to distinguish PTH-mediated from non–PTH-mediated causes. Elevated or inappropriately normal PTH levels suggest primary hyperparathyroidism or familial hypocalciuric hypercalcemia, while low PTH levels prompt evaluation for malignancy, granulomatous disease, vitamin D intoxication, and monoclonal gammopathies through testing such as PTHrP, 1,25-dihydroxyvitamin D, 25-hydroxyvitamin D, SPEP, UPEP, and serum free light chains. Although this algorithm captures the major etiologic categories, it does not include assessment of dietary or non-traditional calcium exposures. 

Our case demonstrates that ingestion of calcium-rich substances, including chalk or culturally rooted forms of kaolin, can lead to significant hypercalcemia and may remain unrecognized without targeted questioning. Adding a step that evaluates dietary practices, cultural ingestion behaviors, and non-nutritive substances could improve detection of these overlooked causes and enhance diagnostic accuracy. 

Pica is managed through a combination of education, nutritional counseling, and behavioral strategies implemented by an interdisciplinary team that may include physicians, nursing staff, psychologists, social workers, dietitians, and family members. Patients and families are taught to focus on understanding the behavior and adopt safer alternative coping skills.7

Conclusion

This case illustrates the importance of considering nontraditional and dietary sources of calcium in the evaluation of severe hypercalcemia and hypercalcemia-induced pancreatitis. Uncommon etiologies such as chalk ingestion can be easily overlooked without targeted questioning, particularly when the clinical picture remains unexplained after routine evaluation. Adding this step to clinical algorithms may facilitate earlier recognition of atypical causes, prevent delayed diagnosis, and improve patient outcomes. 

References

1. G, Kui B, Hegyi P, et al. Hypercalcemia Causes More Severe Acute Pancreatitis: An International Multicenter Cohort Study. Journal of Clinical Medicine. 2025;14(17):6304. doi:10.3390/jcm14176304.

2. Carroll MF, Schade DS. A practical approach to hypercalcemia. Am Fam Physician. 2003;67(9):1959–1966. PMID:12751656

3. Walker MD, Shane E. Hypercalcemia: A Review. JAMA. 2022;328(16):1624-1636. doi:10.1001/jama.2022.18331.

4. Danese A, Lippi G. Milk-alkali syndrome: a systematic review. Clin Cases Miner Bone Metab. 2012;9(3):122–125. PMID: 23269887

5. National Library of Medicine. Calcium Carbonate. Nih.gov. Published 2019. https://pubchem.ncbi.nlm.nih.gov/compound/Calcium-carbonate

6. Grigsby RK, Thyer BA, Waller RJ, Johnston GA Jr. Chalk eating in middle Georgia: a culture-bound syndrome of pica? South Med J. 1999 Feb;92(2):190-2. doi: 10.1097/00007611-199902000-00005. PMID: 10071665.

7. Sayetta RB. Pica: an overview. Am Fam Physician. 1986; 33:181–185.

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Frontiers in Endoscopy, Series #103

Ergonomics in Endoscopy

February 2026 • Volume MMXXVI, Issue 2
Christina M. Minami,Douglas G. Adler

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Introduction 

Musculoskeletal injuries are prevalent among healthcare workers. Proceduralists, such as gastroenterology (GI) endoscopists, require repetitive and often unnatural movements while maneuvering endoscopes and colonoscopes. The frequent stress and forces naturally lead to injuries and pain. Currently the one-size-fits-all endoscopes do not accommodate for the various hand sizes and body types of endoscopists. Proper ergonomics during procedures are recommended to both prevent and ameliorate endoscopy related injuries. The purpose of this article is to review the current literature on published studies and recommendations for gastroenterologists regarding ergonomics in endoscopy.

Injuries in Endoscopy

The most common sites of pain among endoscopists varied between studies. The most frequent sites of pain were low back, hand and wrist, fingers, neck, right shoulder, and left thumb.    The left thumb is particularly exerted during both colonoscopy and ERCP, of note. In an electronic survey sent to 72 GI physicians and 104 non-GI physicians employed by Mayo Clinic, frequency of overall musculoskeletal (MSK) pain was not significant between the two groups, but frequency of pain in left thumb, hand, and wrist were significantly higher in the GI group.2 Endoscopists in practice less than 39 months experienced more left thumb and finger pain, while endoscopists practicing longer most commonly experienced left shoulder pain.1 In a Canadian survey of 133 physicians practicing ERCP in Ontario, 74% of endoscopists attributed their pain to procedure work, and yet only 18% of participants modified their work based on their pain or injuries.3 

Injuries from endoscopy can be serious and debilitating. In a survey of 171 endoscopists of the Portuguese Society of Gastroenterology, missing work due to musculoskeletal injury was reported by 10.1% of respondents and 33.6% required a reduction in physical activity outside of work.

Risk Factors

The literature suggests a higher risk for injury in females compared to males, although studies seem to differ on statistical significance. This may be due to physical differences in hand sizes between males and females, as the endoscope is of constant size regardless of the user. (Figure 1) With the increasing number of women entering the field of gastroenterology, in 2020, Bhatt et al. distributed an electronic survey which sought to evaluate the subtle gender differences in endoscopy ergonomics. They found a statistically higher incidence of injury in females compared to males (p = 0.02) and a higher incidence of wrist pain in females compared to males (p = 0.02). This was the first study to show, with statistical significance, differences in injury by gender. It was attributed to disproportionately smaller hand/glove size, and lesser muscle mass and upper body strength compared to males. On the other hand, in a large electronic survey of 1,698 members of the American College of Gastroenterology, the authors found no significant differences in prevalence of endoscopy related injury in men compared to women (p = 0.77). The authors did find that females were more likely to have upper extremity and upper back pain. 

During endoscopy, the proceduralist must often hold and repeat difficult movements again and again, frequently in awkward positions, alternately pinching, gripping, pushing, pulling, and torquing the endoscope and its accessories for the entirety of the procedure. Bhatt et al. also found that females, compared to their male counterparts, tended to hold the endoscope umbilical cord outside the forearm (p = 0.00), use the right hand to turn the small wheel (p = 0.03), and were more likely to use a pediatric colonoscope in smaller patients (p = 0.01). (Figure 2) This was likely attributed to females with smaller body and hand sizes needing to bear the weight and diameters of the endoscope and apply adequate force during the procedure. Regarding turning and stabilizing the endoscope shaft itself, they found no significant difference in technique between men and women (p = 0.26). To turn the scope, most endoscopists (94.5%) favored torquing or twisting the shaft. Other less frequently used techniques included turning the left forearm which holds the endoscope control head (47.4%), using the small wheel for left or right deflection (45.8%), and turning their entire body (41.1%). To stabilize the endoscope shaft, most endoscopists chose to either place the shaft on the bed (67.3%) or stabilize the shaft with their body (65.4%). Other less common techniques to stabilize the shaft included holding it between the fingers of the left hand (49.5%) and asking for assistance from a technician or nurse (28%).5 

These maneuvers place significant strain on the endoscopist’s musculoskeletal system. Shergill et al. quantified this strain by measuring the thumb force and forearm muscle loads of the extensor carpi radialis and flexor digitorum superficialis during colonoscopy insertion versus withdrawal. Tactile thumb pads were used to measure thumb force and bilateral muscle electromyography (EMGs) were used to measure muscle loads. They evaluated 12 attending gastroenterologists from the University of California, San Francisco and found that forearm loads were significantly greater during insertion even though more time was spent during withdrawal (p <0.05). Highest thumb forces also occurred during colonoscopy insertion compared to withdrawal. 

Injury may start as early as gastroenterology fellowship and becomes more likely over time. These early stages of training and introduction to endoscopy are crucial for learning proper posturing and techniques to reduce physical strain. In a study attempting to assess the prevalence of MSK injuries among GI fellows across the United States, 47% of 156 survey participants experienced new endoscopy-related MSK injury during fellowship and 85% occurred within the first 12 months. In a similar survey analyzing the prevalence of endoscopy-related overuse injuries in GI fellows (n = 165), 20% reported a musculoskeletal injury with female gender as the only factor associated with a higher rate of injury. These injuries may be subsequent results of improper positioning of the patient and/or the monitor, and/or improper endoscopic technique. 

Working as an attending in a fellowship program may be a protective factor, as Bhatt et al. found that working with GI fellows decreased the risk of injury significantly, suggesting a decreased endoscopy workload may be beneficial.5

In a Japanese web-based survey focusing on sites of injuries and risk factors among 352 Japanese endoscopists, they found that greater than or equal to 28 endoscopy procedures per week and age older than 36 years old were associated with endoscopy related injury. Endoscopist height taller than or equal to 172 cm was associated with neck injuries in males. Specifically, for hand injuries, risk factors included glove size greater than or equal to 7 in males and age above 36 in females. Authors suggested that in males, hand size does not always match the standard size of endoscope. Additionally, their study showed that most females were also dissatisfied with the size and shape of the endoscopes. As age increases in females, arthritis is precipitated or worsened by frequent pinching and gripping. They concluded that changing the endoscope design and operability may be essential in preventing endoscopy-related injury.

Proper Ergonomics

To follow proper endoscopy ergonomics, the American Society of Gastroenterology Endoscopy (ASGE) suggests ergonomic education to reduce risk of endoscopy related injury. Hansel et al. recommends aiming to reduce twisting and bending during procedures, having adjustable table heights to allow the endoscopist’s elbows to be gently flexed at approximately 90 degrees, video monitors side by side with the endoscopist’s eyes at three-quarters the way up the screen, using two-piece lead aprons (as opposed to one-piece aprons), scheduled breaks between procedures, and floor padding.2 Similarly, Khan et al. recommended that the video monitor should be directly in front of the endoscopist, 15-25 degrees below eye level, the bed height between elbow height and 10 cm below elbow height, keeping foot pedals in front of the endoscopist’s body, cushioned floor mats, two-piece lead aprons, endoscopists keeping in neutral position and square to monitor with feet hip-width apart, and finger grip 15-30 cm from anorectum when colonoscopy was being performed. (Figures 3 and 4) Markwell et al. created individualized wellness plans for eight Duke University gastroenterologists at an ambulatory surgical center. They recommend a monitor height 15 degrees below the horizontal visual field, monitor placement directly in front of the physician to reduce cervical strain while maintaining clarity, bed at a height to allow the right hand to be at elbow height to 10 cm below elbow height, ergonomic floor mats, and closed toe footwear with arch support.

Prevention

Making Modifications

Modifications can, and should, be made to prevent and treat endoscopic injuries. Comparing the 109 endoscopists to the 120 non-endoscopists in Kuwabara et al.’s study, the endoscopists chose to make fewer modifications to their daily practices to prevent musculoskeletal pain. The reasons for this were unclear, but it was speculated to be due to limited time, busier schedules, or a lack of willingness. In this study, the endoscopists’ most common request to improve endoscope design was making parts of the endoscope lighter and smaller.1 In a  survey by Bhatt et al. more female participants, as compared to male participants, were willing to try a pre-procedure posture checklist, wear a posture sensor to signal the endoscopists to stand up straight, and use braces at sites of pain. This may be attributed to the significantly higher rate of injury in the females included in this study.5 

Hansel et al. found that although gastroenterologists and hepatologists employed by Mayo Clinic experienced musculoskeletal injury, nearly a third made no modifications to their practice despite these injuries. Of those who chose to make modifications, the most common choices were stretching, using adjustable height beds, standing on rubber mats, and reducing the overall time spent performing endoscopies.2 The ASGE’s website includes links to the videoGIE journal for stretching suggestions.

It has been suggested that endoscopists do not take enough breaks in prevention of injury. In O’Sullivan et al.’s survey of ERCP endoscopists, more than half of respondents did not take any breaks between procedures.3 

The endoscopists in the study by Shergill et al. were invited to perform simulated colonoscopy using a novel antigravity support arm (zeroG system, Equipois, Manchester, NH, USA). They found that during simulation the support arm decreased muscle activity of the left wrist extensors when evaluated with EMG.7 Another small study of three experienced endoscopists in Bologna, Italy evaluated the advantages of using a lighter, single-use duodenoscope compared with standard reusable ones. They measured upper limb postures and muscle activity, which found that a lighter endoscope could decrease static and dynamic load during ERCP procedures and lower muscle activity.

Multiple studies have attempted to start ergonomics education as early as possible in training. In Pawa et al., gastroenterology fellows who reported no musculoskeletal injuries were significantly more likely to have had previous ergonomics training.8 Khan et al. created a simulation-based ergonomics curriculum studying general surgery, internal medicine, and gastroenterology trainees rotating at St. Michael’s Hospital in Toronto, Canada. This cohort of trainees were compared to a similar group without ergonomics training. In order to quantify musculoskeletal injury, the authors used the “Rapid Entire Body Assessment” (REBA) and “Rapid Upper Limb Assessment” (RULA). These are ergonomic worksheet assessment tools developed to evaluate whole body (REBA) and upper extremity (RULA) ergonomic musculoskeletal injuries., They saw significantly higher REBA scores in clinical colonoscopy (p <0.001) but not significant in simulated colonoscopy. Those without ergonomic training had worse REBA and RULA scores six weeks after training (p<0.001). Similarly, Gala et al. created a six-month curriculum for 37 general GI and fourth year advanced GI fellows. This curriculum included a didactics session based on the ASGE guidelines on ergonomics for prevention of musculoskeletal injury, followed by a session practicing stretches, resistance bands, and ideal postures with a physical therapist. Participants were provided with a lifelong subscription code to the website with home exercises and stretching. They were evaluated with a pre and post curriculum survey. From those who completed post-curriculum surveys, those individuals felt that the interactive session with the physical therapist was the most impactful part of the curriculum. Although there are many studies with a positive response to ergonomics training during fellowship, Villa et al. found differing results. Their 168-participant electronic survey to GI trainees found that 85% of respondents received ergonomics training but found no relation between training and endoscopic related injury.9 

Treatment of Endoscopic Injury

In the study by O’Sullivan et al., the most commonly used treatment for pain and injury from endoscopy included medication (36%), physiotherapy (15%), and massage therapy (13%).3 The University of Miami also created an ergonomics training curriculum for GI fellows incorporating a physical therapist for active practice of exercises and an introduction to a “microbreaks” model. The “microbreaks” model was taken from studies for general surgeons trialing scheduled 1.5-minute breaks at appropriate 20-40 minutes intervals throughout surgical cases. During these breaks, the physician completes exercises and stretches targeting the neck, shoulders, upper back, lower back, wrists, hands, knees, and ankles. This study found that 100% of fellows reported reduction of pain immediately after implementing the “microbreaks” model.,  

Conclusion

Improper ergonomics in GI endoscopy has left many proceduralists with injuries, most commonly in the upper extremity. The literature is mixed on whether females are disproportionately affected by endoscopy related injury, potentially due to smaller statures and hands. Many females report a desire for alternative techniques to accommodate such maneuvers. Injuries from endoscopy start as early as in fellowship training and should be addressed early on. An ergonomic curriculum during training is likely beneficial. During procedures, the patient beds should be at a height allowing the endoscopists elbows bent to approximately 90 degrees, positioning the screen to reduce cervical strain, using floor mats and using two-piece lead aprons when possible. Although there is widespread recognition of ergonomic injury, many gastroenterologists do not make any adjustments to their practice. Proper ergonomics may include making those adjustments before and during procedure, but also planning for microbreaks with stretching and exercises during and after the procedure. In conclusion, GI endoscopists are at risk of experiencing endoscopy-related injuries, and the literature suggests the solution may be multifactorial. The endoscope itself should be modified to accommodate the unique hand and body shapes of endoscopists. Body positioning and equipment positioning should minimize strain or extra force. Breaks and stretching should be incorporated into the proceduralist’s schedule. Finally, formal education on ergonomics should be implemented early in training. 

References

1 Kuwabara T, Urabe Y, Hiyama T, Tanaka S, Shimomura T,
Oko S, Yoshihara M, Chayama K. Prevalence and impact of
musculoskeletal pain in Japanese gastrointestinal endoscopists:
a controlled study. World J Gastroenterol. 2011 Mar
21;17(11):1488-93. doi: 10.3748/wjg.v17.i11.1488. PMID:
21472109; PMCID: PMC3070024.

2 Hansel SL, Crowell MD, Pardi DS, Bouras EP, DiBaise
JK. Prevalence and impact of musculoskeletal injury
among endoscopists: a controlled pilot study. J Clin
Gastroenterol. 2009 May-Jun;43(5):399-404. doi: 10.1097/
MCG.0b013e31817b0124. PMID: 18987554.

3 O’Sullivan S, Bridge G, Ponich T. Musculoskeletal injuries
among ERCP endoscopists in Canada. Can J Gastroenterol.
2002 Jun;16(6):369-74. doi: 10.1155/2002/523125. PMID:
12096300.

4 Morais R, Vilas-Boas F, Pereira P, Lopes P, Simões C,
Dantas E, Cunha I, Roseira J, Cortez-Pinto J, Silva J,
Lage J, Caine M, Rocha M, Flor de Lima M, Costa Santos
MP, Garrido M, Sousa P, Marcos P, Azevedo R, Castro R,
Cúrdia Gonçalves T, Leal T, Magno-Pereira V, Ramalho R,
Rodrigues-Pinto E, Macedo G. Prevalence, risk factors and
global impact of musculoskeletal injuries among endoscopists:
a nationwide European study. Endosc Int Open. 2020
Apr;8(4):E470-E480. doi: 10.1055/a-1038-4343. Epub 2020
Mar 23. PMID: 32258368; PMCID: PMC7089795.

5 Bhatt A, Patil P, Thosani NC. Endoscopy ergonomics:
a survey-based study exploring gender differences.
Gastrointest Endosc. 2024 Jul;100(1):17-26. doi: 10.1016/j.
gie.2024.01.003. Epub 2024 Jan 6. PMID: 38185181

6 Pawa S, Banerjee P, Kothari S, D’Souza SL, Martindale
SL, Gaidos JKJ, Oxentenko AS, Burke CA; Women in
Gastroenterology Committee of the American College
of Gastroenterology. Are All Endoscopy-Related
Musculoskeletal Injuries Created Equal? Results of a National
Gender-Based Survey. Am J Gastroenterol. 2021 Mar
1;116(3):530-538. doi: 10.14309/ajg.0000000000001136.
PMID: 33560650.

7 Shergill AK, Rempel D, Barr A, Lee D, Pereira A, Hsieh
CM, McQuaid K, Harris-Adamson C. Biomechanical risk
factors associated with distal upper extremity musculoskeletal
disorders in endoscopists performing colonoscopy.
Gastrointest Endosc. 2021 Mar;93(3):704-711.e3.
doi: 10.1016/j.gie.2020.11.001. Epub 2020 Nov 5. PMID:
33160978.

8 Pawa S, Martindale SL, Gaidos JKJ, Banerjee P, Kothari S,
D’Souza SL, Oxentenko AS, Burke CA. Endoscopy-related
injury among gastroenterology trainees. Endosc Int Open.
2022 Aug 15;10(8):E1095-E1104. doi: 10.1055/a-1869-
9202. PMID: 36032041; PMCID: PMC9403520.

9 Villa E, Attar B, Trick W, Kotwal V. Endoscopy-related
musculoskeletal injuries in gastroenterology fellows. Endosc
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5985. Epub 2019 Jun 12. PMID: 31198844; PMCID:
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10 K, Schoenberger H, Sesto M, Gaumnitz E, Teo Broman A,
Saha S. Musculoskeletal Injuries Are Commonly Reported
Among Gastroenterology Trainees: Results of a National
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11 Ono S, Nakajima S, Owada S, Tomita N, Tsuda M, Yamada
M, Katsuki S, Sakamoto N. A Survey on Endoscopy-Related Musculoskeletal Injuries in Japanese Endoscopists
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12 Pawa S, Kwon RS, Fishman DS, Thosani NC, Shergill
A, Grover SC, Al-Haddad M, Amateau SK, Buxbaum
JL, Calderwood AH, Chalhoub JM, Coelho-Prabhu N,
Desai M, Elhanafi SE, Forbes N, Fujii-Lau LL, Kohli DR,
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Thiruvengadam NR, Qumseya BJ; (ASGE Standards of
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13 Khan R, Faggen A, Shergill A, Grover SC, Walsh CM.
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2023 Feb 14. PMID: 36804733.

14 Markwell SA, Garman KS, Vance IL, Patel A, Teitelman M.
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15 Chang MA, Mitchell J, Abbas Fehmi SM. Optimizing ergonomics
after endoscopy. VideoGIE. 2017 Apr 10;2(7):171.
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16 Cennamo V, Botter A, Landi S, Graziosi F, Bassi M, Dabizzi
E, Ghersi S, Cerone G, Bonfiglioli R. Can single-use versus
standard duodenoscope improve ergonomics in ERCP? A
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17 Ergo Plus: A step-by-step guide to the REBA assessment
tool. Available at: https://ergo-plus.com/reba-assessmenttool-
guide

18 Ergo Plus: A step-by-step guide to the RULA assessment
tool. Available at: https://ergo-plus.com/rula-assessmenttool-
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19 Khan R, Scaffidi MA, Satchwell J, Gimpaya N, Lee W,
Genis S, Tham D, Saperia J, Al-Mazroui A, Walsh CM,
Grover SC. Impact of a simulation-based ergonomics training
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20 Gala K, Ghusn W, Coelho-Prabhu N, Wang XJ.
Implementation and Evaluation of a Curriculum for
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2023 Dec;68(12):4301-4305. doi: 10.1007/s10620-023-
08111-z. Epub 2023 Oct 10. PMID: 37815687.

21 Sussman M, Sendzischew-Shane MA, Bolanos J, Deshpande
AR, Kerman D, Allespach H. Assurance for Endurance?
Introducing a Novel Ergonomics Curriculum to Reduce Pain
and Enhance Physical Well-Being Among GI Fellows. Dig
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020-06406-z. PMID: 32548812.

22 Park, Adrian E. MD, FACS; Zahiri, Hamid R. DO; Hallbeck,
M. Susan PhD; Augenstein, Vedra MD, FACS; Sutton,
Erica MD, FACS; Yu, Denny PhD; Lowndes, Bethany R.
BS; Bingener, Juliane MD, FACS. Intraoperative “Micro
Breaks” With Targeted Stretching Enhance Surgeon Physical
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10.1097/SLA.0000000000001665

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NUTRITION REVIEWS IN GASTROENTEROLOGY

Thank You to the 2025 Peer Reviewers of the Nutrition Reviews in Gastroenterology Series

January 2026 • Volume MMXXVI, Issue 1
Neha D. Shah,Elizabeth Wall

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Thank you to the 2025 Peer Reviewers of the Nutrition Reviews in Gastroenterology Series
We extend our sincere appreciation to the reviewers of the 2025 Nutrition Reviews in
Gastroenterology series for their thoughtful and scholarly critique of manuscripts. Their
expertise, time, and thoughtful contributions are vital to the scientific publication process.

We thank:

Amber Antonopoulos, RD, CNSC

Lori Beeken, MS, RDN

Lauren Cornell, MS, RD, CSDH

Gabriela Gardner, PSM, RD-AP, LD, CNSC, CSDH

Anne Guinane, MS, RD, LDN, CNSC, CCTD

Erin Judge, RDN, LDN

Christopher Kasia, MD

Alyssa Lavy, MS, RD, CDN, CSDH

Laura Manning, MPH, RDN, CDN, CSDH

Kate Mintz, MS, RD

Marcia Nahikian-Nelms, PhD, RDN, FAND

Monica Nandwani, DNP, RN, FNP-BC, NEA-BC

Kelly Roehl Nawakowski, MS, RDN-AP, CNSC

Megan Prochaska, MD

Beth Rosen, MS, RD, CDN, CSDH

Christine Scarcello, MS, RD, CNSC

Sherry Tarleton, RDN, CNSC, CSDH

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Medical Bulletin Board

American Liver Foundation Celebrates 50 Years of Advancing Liver Health Nationwide

January 2026 • Volume MMXXVI, Issue 1

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Honoring Five Decades of Progress, Commitment, and Support for Liver Patients

(Fairfield, NJ – Jan. 5, 2026) – American Liver Foundation (ALF) proudly announces its 50th anniversary, marking five decades of unwavering commitment to advancing liver health, empowering liver patients and their families, providing groundbreaking public health initiatives and programs, and funding close to $30 million in critical research that supports and educates the 100 million Americans living with some form of liver disease. Since its founding in 1976, ALF has evolved into a leading voice at the forefront of the fight against liver disease, by educating patients and medical professionals through community events, fundraisers and educational webinars and advocating on Capitol Hill for liver health policies. ALF boldly strives to continue forging 50 years forward advancing liver health programs and initiatives that illustrate our continued dedication to liver patients each and every day. 

“ALF has achieved numerous milestones that have shaped the landscape of liver health over the past 50 years, and we’re committed to driving progress 50 years forward to educate and support those battling a liver condition and help end liver disease,” said Lorraine Stiehl, Chief Executive Officer of American Liver Foundation. “As we look 50 years forward, we are excited for each milestone that represents 50 years of stepping stones dedicated to improving the lives of liver patients and their families.”

Key highlights through five decades of innovative growth include:

In the 1980s – ALF established a Research Awards Program that has since awarded close to $30 million to 923 scientists; $2.5M of which was awarded in the last two years alone. ALF unveiled a National Toll-Free helpline, 1.800.GO.Liver (1.800.465.4837), that provides trusted liver health information and support in 50 states today and in over 100 languages; and ALF launched Love Your Liver, its first community education program that taught elementary school children about liver health, resisting peer pressure, and saying no to drugs.

In the 1990s – The first Irwin M. Arias Symposium: Bridging Basic Science & Liver Disease launched, uniting global scientists and physicians to bridge basic science and liver disease. Now in its 35th year, this one-day event has featured breakthroughs in diagnosing and treating liver diseases in children and adults worldwide; ALF convened a Scientific Advisory Council of leading hepatitis and liver disease researchers to draft the nation’s first research agenda, setting priorities for Congress to accelerate cures; ALF published the Children’s Liver Research Agenda: A Scientific Blueprint to help guide families coping with pediatric liver disease; and ALF launched Liver Life Walks to bring communities across the country together to raise awareness and funds regarding liver disease in a fun, inspiring way and to provide education and support services to those living with the disease.

In the early 2000s – ALF launched a multi-year, nationwide community education campaign to raise awareness about Hepatitis B (Hep B) called THINK (The Hepatitis Information You Need to Know); ALF’s Board Chair Dr. James Boyer testified before Congress, advocating for increased funding for the National Institutes of Health (NIH), Center for Disease Control’s (CDC) Viral Hepatitis, and Health Resources and Services Administration’s (HRSA) Organ Transplantation; and ALF launched its third national community education program titled FLIP (Fatty Liver Information Program), which laid the groundwork for what would become ALF’s Liver Wellness Program.

In 2010 to 2020 – Music legends Gregg Allman and Natalie Cole joined ALF’s nationwide Hepatitis C virus (HCV) campaign called “Tune in to Hep C”, to raise awareness about HCV; ALF formed its first-ever National Patient Advisory Committee (NPAC) to train liver patients across the nation to use their voices to advocate for change and raise awareness on Capitol Hill about many liver conditions. Today, ALF hosts an annual advocacy day amplifying many voices to fight for liver health policies during our “Liver Life Advocacy Summit.”; ALF launched a live educational series called Ask the Experts, which brings liver health specialists into communities across the country to raise awareness and answer questions about liver health; ALF honored 2020 Nobel Laureates Charles M. Rice, PhD, Harvey Alter, MD, and Michael Houghton, PhD, DSc, at ALF’s 45th Anniversary Leadership Celebration for their discovery of the hepatitis C virus and transformative contributions that led to a cure.

In 2020 to the present – ALF launched Think Liver Think Life, it’s first nationwide public health initiative to screen U.S. adults for metabolic dysfunction-associated steatotic liver disease (MASLD) and liver cancer, raising awareness and connecting communities to the care they need. See if you’re at risk today by  taking our free liver health quiz at thinkliverthinklife.org/quiz; ALF created the Bili the Brave toolkit, complete with a plush lion, children’s book, and resources to support children and families affected by biliary atresia; ALF’s Living Donor Network was recently launched to connect non-directed (altruistic) liver donors with transplant centers nationwide to help children and adults in need of a transplant; and ALF launched a Patient Registry to help researchers find better treatments and cures for liver disease.

“ALF expresses profound gratitude to its donors, volunteers, medical partners, scientists and researchers and the liver health community for their steadfast support of our mission for the past 50 years,” said Emmanual Thomas, MD, PhD, FAASLD, ALF Board Chair and Tenured Professor at University of Miami School of Medicine and member of the Sylvester Comprehensive Cancer Center and the Schiff Center for Liver Diseases at University of Miami. “As ALF celebrates its legacy, we look 50 years forward with renewed commitment to fostering hope, advancing innovative breakthroughs, and supporting millions affected by liver disease.”

In honor of our 50th Anniversary milestone, ALF invites all its supporters to join the Liver of Life Society with a monthly donation of $15 or more. By becoming a monthly donor, you can make a lasting difference in the fight against liver disease that will help us sustain vital programs year-round. As a token of our appreciation, all Liver of Life Society members will receive ALF’s commemorative 50th Anniversary tote bag.

“For the past 50 years, ALF has continued to be a beacon of hope for liver patients across the country living with some form of liver disease,” said Dan Weil, immediate past Board Chair of ALF, and spouse to a liver patient for over 25 years. “ALF’s goal is to create a world free from the challenges of liver disease, but we can’t do it without your continued support of our ongoing mission to promote education, advocacy, support services and research for the prevention, treatment and cure of liver disease. Supporting ALF today means you’re helping millions in the future to lead healthier lives and achieve optimal liver health.”

For more information about ALF, go to www.liverfoundation.org and for details regarding the Monthly Donor Campaign, please visit Liver of Life Society – American Liver Foundation. Read ALF’s entire 50th Anniversary timeline. If you have any questions or concerns regarding liver disease, please call our FREE helpline at 1.800.GO.LIVER (800.465.4837).

About the American Liver Foundation

American Liver Foundation (ALF) is a national community of patients, caregivers and medical professionals dedicated to helping people improve their liver health. Providing guidance and life-saving resources, we are a beacon for the 100 million Americans affected by liver disease. We advocate for patients and families, fund medical research and educate the public about liver wellness and disease prevention. We bring people together through our educational programs and events and create a network of support that lasts a lifetime. ALF is the largest organization focused on all liver diseases and the trusted voice for patients and families living with liver disease.

For more information visit:

www.liverfoundation.org

or call: 1 800 GO LIVER (800-465-4837)

SafeHeal® Announces Successful Launch of SAFE-3CV IDE Study for Colovac® Anastomosis Protection Technology

Breakthrough device promises significantly improved patient recovery after colorectal surgery

PARIS, France/Tampa, FL – SafeHeal®, a leading innovator in the field of colorectal cancer surgery, today announced the first patient enrollment in its pivotal IDE study of Colovac®, a groundbreaking endoluminal bypass sheath. Colovac® is intended as an alternative to a temporary diverting ostomy for patients undergoing colorectal resection. Up to 20 U.S. and European sites will enroll patients in the SAFE-3CV study led by Principal Investigator Patricia Sylla, MD, and EU Principal Investigator Prof. Jérémie Lefevre, which is expected to complete enrollment by late 2026. SAFE-3CV serves as the final phase of a comprehensive study for U.S. market approval and EU post-market surveillance. This two-phase study will enroll up to 252 patients to compare the safety and efficacy of the Colovac® device to the previously collected control data on patients who received the standard-of-care diverting ostomy procedure. 

Hôpital Saint-Antoine (AP-HP), Sorbonne Université, Paris, France, under the direction of Prof. Jérémie Lefevre, successfully enrolled the SAFE-3CV study’s first patient.  Prof. Lefevre has extensive experience with the Colovac® device as a co-leader of recent studies conducted in the U.S., Europe, and Asia, where Colovac® has demonstrated favorable safety and efficacy as an alternative to ostomy.  Based on these prior studies, in August 2025, Colovac® was granted European Union marketing approval under the new Medical Device Regulation (EU MDR 2017/745, Medical Devices, Annex IX Chapter I).

“The current standard-of-care, the use of a diverting stoma, places a significant burden on the patient in terms of associated physical complications, lifestyle compromises, and an extended recovery period,” said Prof. Lefevre. “We welcome Colovac’s potential to offer a less-invasive alternative to a stoma, and we are excited to generate additional evidence behind this innovation.” 

As the current standard of care for the surgical treatment of rectal cancer, a diverting ostomy is applied prophylactically to most patients today undergoing a low anterior resection (LAR) and a low anastomosis. The ostomy temporarily diverts the stool away from the healing anastomosis to the outside of the body and into an ostomy bag. In most cases, the ostomy is needed only until the anastomosis has healed, and can then be reversed, typically after 2-6 months. The eventual reversal of the ostomy requires another operation, with a second hospital stay, recovery period and associated complications. In some cases, the ostomy may not be reversed and becomes permanent. In addition to the potential surgical complications associated with ostomy procedures, patients may experience a negative impact on their quality of life due to social isolation, reduced physical activity and/or intimacy issues.

Colovac® is designed to eliminate the need for a temporary stoma in most patients. It aims to improve patient recovery and quality of life by eliminating stoma-related complications, including permanent stoma, and eliminating the physical and emotional burden associated with stoma management and care.

“We are proud to partner with world-class clinicians like Prof. Lefevre and Dr. Sylla to build upon SafeHeal’s already impressive body of evidence, as we drive toward FDA marketing approval of Colovac,” said Chris Richardson, President & CEO of SafeHeal®. “We look forward to making the clinical and economic benefits of this technology available to U.S. patients and providers in the very near future.”

Successful completion of the SAFE-3CV study is the final step in the path to U.S. Food and Drug Administration (FDA) approval and U.S. commercialization of the Colovac® device. The FDA has already granted the product Breakthrough Device designation. Breakthrough Device designation is granted to novel products and provides expedited review of innovative technologies that can improve the lives of people with life-threatening or irreversibly debilitating diseases or conditions.

ABOUT SAFEHEAL®

SafeHeal SAS, headquartered in Paris, France, and its wholly owned U.S. subsidiary, SafeHeal Inc., is a medical device company developing Colovac®, a device intended as an alternative to diverting ostomy in patients undergoing colorectal surgery. Colovac® is a flexible endoluminal bypass sheath designed to reduce the contact of fecal content at the anastomotic site following colorectal surgery. The device is placed endoluminally and remains in place for approximately 10 days, until the body’s natural healing and tissue repair processes are complete, after which it is removed during an endoscopic procedure without the need for a second surgical intervention.

Colovac® enables patients to resume their normal life without the stigma and complications associated with an ostomy procedure. In the U.S., Colovac® is limited by Federal law to investigational use and not currently available for sale.

For more information, please visit:

 www.safeheal.com

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