Category Archives: Pediatric Gastroenterology Intestinal Disorder

Genetic Risk Impacts Severity of Inflammatory Bowel Disease

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MV Vestergaard et al. Gastroenterol 2026; 170: 721-734. Open Access! Genetic Risk of Inflammatory Bowel Disease Is Associated With Disease Course Severity

Methods: The authors calculated IBD polygenic scores (PGS) for 3732 Danish patients with Crohn’s disease (CD) and 4535 patients with ulcerative colitis (UC), and investigated their association with disease outcomes.

“The Danish National Biobank stores neonatal blood spots from almost all Danes born since 1982…The North Denmark IBD (NorDIBD) cohort is a population-based cohort of all patients from the North Denmark Region with a confirmed IBD diagnosis from 1978–2020.17 From this cohort, 940 patients with IBD and a further 973 blood donors with no IBD diagnosis were genotyped from whole blood…applied variant loadings for calculating PGS for CD and UC susceptibility generated by Middha et al19 to our dataset. These variant loadings were derived from summary statistics from the IIBDGC.” This cohort had a young age. Only 2% and 3% of CD and UC patients, respectively, were 40+.

Severe Disease Definitions:

  • For patients with CD, a severe disease course was defined as experiencing (1) 2 or more IBD-related hospitalizations exceeding 2 days, (2) 2 or more IBD-related major surgeries, (3) 1 IBD-related hospitalization and 1 IBD-related major surgery not overlapping in time, or (4) a total use of at least 5000 mg prednisolone-equivalent systemic corticosteroids within the first 3 years after diagnosis
  • For patients with UC the severity definition was modified to experiencing (1) 2 or more IBD-related hospitalizations exceeding 2 days, (2) 1 or more IBD-related major surgeries, or (3) a total use of at least 5000 mg prednisolone-equivalent systemic corticosteroids. 

Key findings:

  • Increased PGS was associated with higher fecal calprotectin and C-reactive protein levels, and decreased hemoglobin levels
  • When comparing the highest vs lowest PGS quintile, we observed a hazard ratio for major surgery of 2.74 in patients with CD and of 2.04 in UC
  • Patients with severe disease had higher PGS than patients with less severe disease (CD, odds ratio = 1.25; UC, odds ratio = 1.33)

The graphs below show the differences in hospitalization and surgery based on PGS for CD (A & B) and then for UC (C & D)

Discussion:

  • “Our results suggest that IBD susceptibility genetics only explain part of the severity of IBD, hence leaving room for other factors at play… This observation is promising, as it points toward the possibility of modulating the effects of genetic susceptibility through lifestyle interventions directed toward potential environmental factors that are yet to be uncovered.”

My take: It is intuitive that those with more genetic risk factors would be more likely to have severe disease. This study shows this assumption is correct in this cohort; in fact, there is a dose-response relationship. Those with higher PGS had more hospitalizations, major surgeries and medical treatments.

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Most Common Symptoms with a Gluten Challenge in Those with Celiac Disease

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M Banegas et al. Am J Gastroenterol 2026; 121: 501-516. Open Access! Gastrointestinal and Extraintestinal Symptoms Among Subjects With Celiac Disease Undergoing a Dose-Specified Gluten Challenge: A Systematic Review and Meta-Analysis Thanks to Ben Gold for this reference.

Methods: In this review/meta-analysis with 35 eligible studies, there were 1,002 adult participants with celiac disease (CeD) in remission on a gluten-free diet undergoing a gluten challenge (GC).

Key findings:

  • The most common symptoms were abdominal pain (41-56%), bloating (37-55%), and nausea (34-41%). The lower numbers were the composite result from non-randomized controlled trials; the higher numbers were reported in randomized controlled trials
  • Diarrhea was reported in 29-38%
  • Bloating, fatigue, flatulence, and nausea were significantly more reported in studies administering ≥6 g gluten/d

My take: The symptoms that occur with a gluten challenge are likely similar to those with inadvertent intake. However, with inadvertent gluten exposure, the amount of gluten could be substantially more and increase the severity of symptoms.

Eosinophilic Esophagitis: “Fifth Member of the Atopic March”

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Since I completed my pediatric residency and pediatric gastroenterology fellowship in Cincinnati, I receive their bulletins. A recent title (Link: EoE: The Fifth Member of the Atopic March) prompted me to review the source article. The Cincinnati summary noted that “children with AD [atopic dermatitis] within the first two years of life are 10 times more likely to develop EoE [eosinophilic esophagitis] by age 8.”

Source article: WC Chang et al. Journal of Allergy and Clinical Immunology 2026; 157: 999-1001. Open Access! Longitudinal enrichment of eosinophilic esophagitis in children with AD: The MPAACH cohort

Background: The atopic march refers to the natural history of allergic disease manifestations as they develop in childhood.1 Classically, the march begins with atopic dermatitis (AD), followed sequentially by food allergy (FA), asthma, and allergic rhinitis (AR),1 but there is significant heterogeneity in the timing, order and organ(s) affected.2 

Methods: Using the Mechanisms of Progression of Atopic Dermatitis to Asthma in CHildren (MPAACH) cohort,4 a US longitudinal early-life cohort of children (n=700) with AD, the authors examined the associated epidemiology of EoE with other members of the atopic march.

Key findings:

  • “Of 700 MPAACH participants, 10 have EoE, and in all cases, EoE developed after AD onset. Of these 10 subjects, 2 had EoE at enrollment, whereas 8 developed EoE subsequent to enrollment in MPAACH”
  • “To date, 48.9% of the children in MPAACH had developed at least 1 allergic comorbidity (FA, AR, and/or asthma) by age 8 years versus 90% of the children with EoE (P = .009), highlighting the strong association between EoE and other atopic diseases”
  • “Despite no difference in skin barrier quality or AD severity, the children with EoE were significantly more likely to have food sensitization (as defined by at least 1 positive result of a skin prick test to a food allergen [60% vs 28% (P = .039)]) and FA (70% vs 13% [P < .001])…suggesting that the esophageal epithelium may be the site of allergen penetration and immune activation, independent of the skin barrier” 

My take: There was a 10-fold higher risk of EoE (1.4% or 10 of 700) in this cohort of children with AD compared to the general population. However, I was expecting a much higher prevalence in this population. This could be due to the fact that patients are seeing me for GI symptoms rather than for AD. It is possible, as well, that the number of EoE patients would be higher if there was a prospective evaluation (e.g. endoscopy).

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Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician.  Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition

Position Paper: Expediting Drug Approval for Pediatric IBD

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D Turner et al. J Pediatr Gastroenterol Nutr. 2026;82:867–894. Reshaping study design for faster extrapolation‐baseddrug approval in pediatric inflammatory boweldiseases: An ESPGHAN–NASPGHAN position paper

“It has been 11 years since the adult approval of vedolizumab and 9 years since the approval of ustekinumab, yet neither is currently approved for use in children (Table 1). Instead of taking the necessary steps to shorten this unacceptable delay, there are now extra hurdles for clinical trials such as three ileocolonoscopies over 1 year in both pediatric CD and UC, as suggested by the FDA…”

Addendum: See comment by Matthew Kowalik, MD who is the Director (Acting) of Division of Gastroenterology for FDA/CDER/OND/OII. There has been recent approval recent of Stelara (ustekinumab) for the treatment of pediatric patients 2 years and older with moderately to severely active Crohn’s disease. Here’s a link: Johnson & Johnson (JNJ) Gains FDA Approval for Pediatric Crohn’s Disease Treatment

“Pediatric extrapolation is based on assessing relevant similarities in disease characteristics, drug pharmacology, and treatment response between the target pediatric population and adults or other reference pediatric populations. While, historically, extrapolating safety data was considered unacceptable, the recent International Council for Harmonization (ICH) E11A Guideline on pediatric extrapolation that has been endorsed in 2024 by the EMA”[European Medicines Agency (EMA) ]

Selected Summary Statements (total of 24 are in the report):

  • 1.There is no evidence that differences in pathogenesis and pathobiology between pediatric and adult patients with IBD are associated with differences in response to pharmaceutical therapies, except for monogenic disease (agreement 21/22).
  • 2.In general, efficacy and drug-related safety outcomes in children older than 2 years are comparable to adults (agreement 22/22).
  • 9. Optimal dosing should be used in all study arms in pediatric trials. Placebo, sham, or doses demonstrated to be subtherapeutic in prior studies should not be permitted. They are unethical in children, reduce feasibility of enrollment, and are not expected to be informative given the underpowered sample size of pediatric studies (agreement 22/22).
  • 13.Ileocolonoscopic assessment is the gold standard for assessing mucosal healing (MH) and should be required at most twice in each study: that is, at baseline and study end (agreement 22/22).
  • 14. Noninvasive objective measures, including serum and fecal biomarkers, magnetic resonance enterography (MRE), and/or intestinal ultrasound (IUS), should be used for assessing postinduction interim therapeutic response between the two ileocolonoscopies rather than requiring a third ileocolonoscopy (agreement 22/22).

My take (borrowed from the authors):

  • “While it is paramount to achieve a precise and comprehensive approval process for new drugs in pediatric IBD, it is equally important to expedite the process, so children and adolescents are not denied effective treatment available for adults with IBD…”
  • “Under these assumptions, future trial designs should be single-arm and open-label to focus on dosing and pharmacokinetics in children weighing <30–40 kg while mandating long-term safety registries, disease- and not necessarily drug-specific. Data should be supported by meticulously collected real-world evidence. Pediatric data must be collected as soon as a confident signal of efficacy and safety is achieved in adult studies…”
  • “This will resolve the current paradox in which children have the most severe and extensive disease and the highest efficacy of drugs, yet very limited access to these drugs.”

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Upadacitinib for Pediatric Ulcerative Colitis

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A Yerushalmy-Feler A et al. Clinical Gastroenterology and Hepatology, 2026 (In press); Upadacitinib Maintenance Therapy in Pediatric Ulcerative Colitis: 52-Week Multicenter Study From the Porto Group of the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition

Background/Methods: There is limited data on the use of upadacitinib for pediatric inflammatory bowel disease. This retrospective data from 35 European centers analyzed its effectiveness in 105 children (95 with UC and 10 with IBD-U).  Prior to upadacitinib, 103 of 105 children (98%) were treated with biologic therapies and 79 (75%) with ≥2 biologics. The induction dose was 45 mg in 86% of cohort; the maintenance dose was 30 mg in 87% (only 2 patients received 45 mg maintenance). Mean age at IBD diagnosis was 11.3 yrs and mean age at start of upadacitinib was 14.6 yrs. 65% of study participants had a pancolitis.

Key findings:

  • Clinical remission and corticosteroid-free clinical remission (CFR) were observed after 8 weeks in 61 (58%) and 53 (51%) children, respectively
  • By week 52, 75 children (71%) achieved clinical remission, 73 (70%) achieved CFR, and sustained CFR in 63 (60%); CFR with FC <150 mcg/g was reached 30 of 80 (38%) (29% of the ITT group)
  • Adverse effects: There were two serious AEs: an appendiceal neuroendocrine tumor and cytomegalovirus colitis. The most frequent AEs were hyperlipidemia (n = 20), infections (n = 18), and acne (n = 14)

Predictors of response: “The baseline variables that were associated with achieving sustained CFR were prior failure of fewer biologic agents (≤2 vs >2), a lower PUCAI score, absence of corticosteroid therapy, and higher serum hemoglobin and albumin levels.”

Age: “Our findings suggest that upadacitinib provides comparable effectiveness in younger children weighing <40 kg, supporting its therapeutic potential across a broader pediatric age and weight range.”

My take: Upadacitinib is an important therapy for ulcerative colitis in the pediatric age range and in adults. It is effective in all age groups. Also, young children can now be prescribed a liquid version (Rinvoq LQ) which requires twice daily dosing (rather than once a day). Some patients who do not respond adequately or lose response may benefit from higher dosing.

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Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician.  Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

Influencer$ and $upplements (2026)

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Free Link: Sara O’Brien, WSJ 4/226: Would You Spend $1,000 a Month on Supplements?

An excerpt:

Over-the-top supplement regimens have become bragging rights for the health-conscious and wellness-obsessed. From beauty lovers to masculinity influencers, everyone is boasting about their “stacks”—the numerous capsules, powders and injections they take regularly in the hopes of achieving a cumulative, self-optimizing effect. They’re spending over $1,000 a month in some cases on products that purport to improve their sleep, mental health, fertility, appearance and longevity, but often aren’t approved for those purposes. Some are making money from their endorsements….

Supplements went from a means of treating diseases caused by nutritional deficiencies in the 1900s to lifestyle products that are now the backbone of a $70 billion industry. Because they do not undergo approval by the FDA, they aren’t reviewed for safety or efficacy before coming to market. Some have lots of scientific research backing their use, while others have very limited support. Manufacturers are prohibited from making claims about treating or preventing disease, but influencers have sold the idea that buying the right products can fend off or cure almost any ailment…

Nutritionists generally recommend filling nutrient gaps through food rather than supplements when possible. Some supplements can actually introduce or exacerbate health issues. 

“It’s a new addiction that people have,” said Mona Sharma, a celebrity nutritionist in Los Angeles. She said many of her clients take upward of 15 supplements a day. One female client, she said, was taking 70 of them, following guidance she’d seen online, without feeling any positive effect on her well-being. 

My take: Supplements are a $70 billion/year industry, with no proven benefit in healthy individuals; yet, these products are promoted heavily by thousands of paid influencers. Many of the same people who are taking and/or promoting supplements oppose vaccines, when only the later has extensive evidence of benefits.

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Highlights from Eric Topol, MD

Lasting Effects of Antibiotics

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Baldanzi, G., Larsson, A., Sayols-Baixeras, S. et al.  Nat Med (2026). https://doi.org/10.1038/s41591-026-04284-y. Open Access! Antibiotic use and gut microbiome composition links from individual-level prescription data of 14,979 individuals.

This is a highly-detailed and lengthy report (25 pages).

Methods: The authors combined individual-level data from the Swedish Prescribed Drug Register with fecal metagenomes of 14,979 adults to examine the association between oral antibiotic use over 8 years and gut microbiome. The authors used several microbiome diversity metrics.

Key findings:

  • Antibiotic use <1 year before fecal sampling was associated with the greatest reduction in species diversity, but significant associations were also observed for use 1–4 and 4–8 years earlier. 
  • Clindamycin, fluoroquinolones and flucloxacillin accounted for most of the associations with the abundance of individual species. Use of these antibiotics 4–8 years earlier was associated with altered abundance of 10–15% of the species studied

My take: Clindamycin, fluoroquinolones and flucloxacillin had the largest and most persistent effects on the microbiome. The significance of these microbiome disruption is not clear; though, there have been reports of an association of increase use of antibiotics with cardiovascular disease, inflammatory bowel disease, celiac disease, type 2 diabetes, and colorectal cancer. An association with these disorders, however, does not prove causality.

From the authors: “the primary reason for a restrictive use of antibiotics is the risk of resistance development. Still, our study adds another argument for reducing antibiotic use: namely, gut microbiome alterations that may persist for many years. As the microbiome field advances, our understanding of the long-term impact of antibiotic treatment beyond infections and resistance may reveal additional health implications.”

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AAP & NASPGHAN: Practice Guideline for Faltering Weight

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HB Kersten, PS Goday et al. PEDIATRICS Volume 157, Issue 4, April 2026:e2025075764. Open Access! PDF: Clinical Practice Guideline for Diagnosis and Management of Faltering Weight

The AAP in partnership with the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN) has published its first clinical practice guideline on diagnosis and management of “faltering weight,” a condition formerly described as “failure to thrive” that affects 5%-10% of young pediatric patients in the primary care setting.

  • The clinical practice guideline (CPG) explains that the prior term, failure to thrive (FTT), has never been well-defined. In addition, “the term FTT has also been fraught with controversy that has contributed to the difficulty in determining the criteria used to define it. The word “failure” has led caregivers to feel blamed for their child’s condition. The term has also
    been inconsistently applied, which may exacerbate existing health care inequities.”
  • “When evaluating a child who has been hospitalized for faltering weight, consider the 5 most-common co-occurring conditions…congenital heart disease, gastroesophageal reflux disease (GERD), swallow dysfunction, neurologic disease, genetic abnormalities/congenital syndrome.”
  • “When evaluating a child in the outpatient setting for faltering weight, consider the 5 most-common co-occurring conditions….gastrointestinal disease, pulmonary disease, food allergy, genetic abnormalities/congenital syndrome, neurologic disease.”

My take: Overall, this is a useful guideline. A couple comments:

  1. For several decades I have avoided the term ‘failure to thrive’ (for the reasons given in the CPG) and typically have used terms like poor weight gain or growth failure.
  2. Most pediatric patients with faltering weight need to ingest more calories and do not need extensive testing. I agree that endoscopy should not be part of the routine workup for faltering weight in the absence of other indications
  3. “Gastroesophageal reflux disease” is often attributed as a reason for faltering weight as well as choking. However, isolated reflux is unlikely to cause these presentations in the absence of other factors (e.g. pyloric stenosis, malrotation, swallow dysfunction)

Additional Links:

Clinical Practice Guideline

Technical Reports

AAP News coverage

Information for Families from HealthyChildren.org

  • Faltering Weight in Children: Parent FAQs, in English and Spanish
  • Understanding Growth Charts: A Parent’s Guide to Percentiles & Z-Scores, in English and Spanish

Further reading

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Dr. Danielle Wendel: Management of Short Bowel Syndrome

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Two years ago, Dr. Wendel gave our group a great lecture on short bowel syndrome (SVS). One of the neonatologists in attendance invited her back to provide a state of the art update. While this 2026 lecture covered some of the same issues, there were important updates and insights.

My notes below may contain errors in transcription and in omission. In addition, the information provided is based on what is done in Seattle. However, there is not a lot of evidence for much of what is done in intestinal rehabilitation. Thus, there is variation in practice at different centers and what works for one patient might not work for another. Following my notes, I have included many of her slides.

Diet:

  • Enteral feedings promote intestinal adaptation. Pediatric patients with SBS require much higher calories with enteral nutrition and may have hyperphagia as a compensatory mechanism
  • Breastmilk and/or Standard formula likely help promote intestinal adaptation better than hydrolysates and elemental formulas. In addition, it may help reduce the development of food allergies which are increased in children with SBS
  • Oral feedings have many advantages over NG or GT feedings when feasible. The ability to consume solid foods is quite helpful in reducing diarrhea. Also, encouraging oral feedings may help reduce feeding aversions. As such, GT placement is avoided if possible in Seattle
  • Key diet advice: avoid sweet tasting food/drink, especially in the first few years of life while they are developing their palate/food preferences
  • Feed osmolarity/caloric density: Most children with SBS tolerate lower caloric density (15-20 cal/oz) and more volume orally rather than higher caloric density/lower volume feeds

Parenteral Nutrition:

  • Lipid emulsions: SMOFlipid at 2 gm/day can help prevent essential fatty acid deficiency (EFA). Omegaven may need to be dosed at 1.5 gm/day to prevent EFA. If used for short-term and low dose, standard intralipid can be useful
  • HAL (aka TPN): Typically weaning calories is done before weaning volume. Cycling HAL (delivering over fewer hours) can be started prior to discharge. Watch for tolerance of the glucose infusion rate (JH: I prefer the terms HAL = hyperalimentation or PN=parenteral nutrition. TPN =total parenteral nutrition. Most patients are receiving parenteral nutrition but not total parenteral nutrition.)

Ostomy/Stool Output:

  • Output goals: Most pediatric patients can tolerate output of 50 mL/kg/day of ostomy output  (if being supported by PN), though less than 30 mL/kg/day is more physiologic
  • Iron: Parenteral iron is typically needed. Seattle team prefers ferric carboxymaltose as it may deliver enough iron for 6-12 months in one infusion
  • Acid suppression: While acid suppression can sometimes be beneficial by lowering gastric output, if possible avoid long-term use as it may increase risk of bacterial overgrowth along with other infections
  • Excessive stool output (via stoma or per rectum) is when it is more than the patient’s baseline. This should prompt investigation for potential causes including diet/osmotic agent, bacterial overgrowth and infections
  • Pancreatic enzymes: It is unclear if pancreatic enzymes (PERT, Relizorb) will improve stool output due to lack of data
  • Teduglutide can reduce the need for HAL. It is a hormone (like insulin) and sustained effects are generally not seen when it is stopped. However, especially in patients close to coming off HAL, it may be beneficial

Monitoring:

  • Nutrient deficiencies: Close monitoring for nutrient deficiencies is needed and often even more important when no longer receiving HAL
  • Urine sodium more than 30 is a goal. Sodium depletion interferes with growth and can contribute to other electrolye disturbances (eg. hypokalemia)

CLABSI:

  • Antibiotics: Treatment starts with a broad-spectrum antibiotic and wait to add specific gram-positive coverage unless ill-appearing or gram-positive organism starts growing. Vancomycin is not used frequently in Seattle due to concerns of renal toxicity. In patients with gram-positive infection, linezolid is often used
  • Minimum of 48 Hours For All Fevers: Everyone with SBS and with fever (greater than or equal to 100.4) stays for at least 48 hrs on broad spectrum IV antibiotics
  • Locks: Sodium bicarb locks help prevent CLABSI and appear to have similar infection prevention as ethanol locks. Ethanol locks have been difficult to get coverage.

SIBO:

  • Medications: Metronidazole is generally 1st line agent and gentamicin (IV formulation given enterally) is a 2nd line agent in Seattle. Rifaximin would be potentially their 1st line agent if it were easier to get covered

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Disclaimer: This blog, gutsandgrowth, assumes no responsibility for any use or operation of any method, product, instruction, concept or idea contained in the material herein or for any injury or damage to persons or property (whether products liability, negligence or otherwise) resulting from such use or operation. These blog posts are for educational purposes only. Specific dosing of medications (along with potential adverse effects) should be confirmed by prescribing physician.  Because of rapid advances in the medical sciences, the gutsandgrowth blog cautions that independent verification should be made of diagnosis and drug dosages. The reader is solely responsible for the conduct of any suggested test or procedure.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

Endoscopic Closure of Tracheoesophageal Fistulas in Pediatric Patients

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A Corcoran et al. J Pediatr Gastroenterol Nutr. 2026;82:828–839. Endoscopic tracheoesophageal fistula closure—Electrocautery combined with esophageal clip application in pediatric patients

This retrospective study with 15 patients shows the feasibility of endoscopic closure of tracheoesophageal fistulas (TEFs) in pediatric patients by a highly-specialized multidisciplinary team.

Background: Surgical repair of esophageal atresia (EA) is usually completed in infancy, yet TEF can still be identified later in life. These late-presenting fistulas fall into three general categories .5 First, true recurrences arise when the original site of TEF ligation breaks down, resulting in reformation of the fistula at the prior repair site. These occur in approximately 5%–10% of patients. Second, missed congenital fistulas were present at birth but went undetected during the initial evaluation or operation…Third, acquired fistulas can develop de novo in children without a history of EA, typically resulting from chronic inflammation and tissue breakdown due to an inciting injury, prolonged infection, or a retained foreign body. In children with repaired EA, similar fistulas may develop along a new tract months or years after surgery, often arising from the same underlying mechanisms.

Open repair of TEF can be a technically challenging operation, and depending on the location, it requires re-do thoracotomy or neck dissection. Given the morbidity and mortality associated with these open surgical approaches, there has been a growing trend toward endoscopic repair of recurrent, acquired and missed congenital TEF.4–9 

Key findings:

  • in 14 patients, 14 of 15 fistulas were closed successfully
  • Ten TEF were closed with electrocautery and esophageal clip placement while five were closed with cautery alone

Discussion Points:

  • Repeated procedures are often necessary to both achieve and ensure closure for endoscopically treated TEFs.

My take (borrowed from authors): Endoscopic closure using “electrocautery with or without esophageal clip application is a safe, minimally invasive, and effective treatment for all types of TEFs…While especially valuable for patients who are poor surgical candidates due to comorbidities, this approach may also be considered as a first-line option prior to surgical intervention in select cases.”

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View from Victoria Island near Bariloche, Argentina