ACG Clinical Guideline: Diagnosis and Management of Gastrointestinal Subepithelial Lesions.

Subepithelial lesions (SEL) of the GI tract represent a mix of benign and potentially malignant entities including tumors, cysts, or extraluminal structures causing extrinsic compression of the gastrointestinal wall. SEL can occur anywhere along the GI tract and are frequently incidental findings encountered during endoscopy or cross-sectional imaging. This clinical guideline of the American College of Gastroenterology was developed using the Grading of Recommendations Assessment, Development, and Evaluation process and is intended to suggest preferable approaches to a typical patient with a SEL based on the currently available published literature. Among the recommendations, we suggest endoscopic ultrasound (EUS) with tissue acquisition to improve diagnostic accuracy in the identification of solid nonlipomatous SEL and EUS fine-needle biopsy alone or EUS fine-needle aspiration with rapid on-site evaluation sampling of solid SEL. There is insufficient evidence to recommend surveillance vs resection of gastric gastrointestinal stromal tumors (GIST) <2 cm in size. Owing to their malignant potential, we suggest resection of gastric GIST >2 cm and all nongastric GIST. When exercising clinical judgment, particularly when statements are conditional suggestions and/or treatments pose significant risks, health-care providers should incorporate this guideline with patient-specific preferences, medical comorbidities, and overall health status to arrive at a patient-centered approach.

Use of a Second-Generation Irrigation Device May Shorten Time to Successful Inpatient Colonoscopy: A Case Series.

Inpatient bowel preparations are often inadequate, lengthening hospital stay and increasing costs. In this case series, we assessed whether a new irrigation device could shorten times to successful colonoscopy and hospital discharge. The device includes a disposable sleeve fitted over the colonoscope, delivering 4 streams of a pulsed air-water mixture to liquify stool, and contains 2 large-bore suction channels to evacuate fecal material. We present 6 inpatient colonoscopies where the device was used, demonstrating its utility in facilitating timely procedures and efficient patient care. Further study is required to determine whether the consistent use of the device can shorten time to successful inpatient colonoscopy.

Development and Assessment of a New Framework for Disease Surveillance, Prediction, and Risk Adjustment: The Diagnostic Items Classification System.

Importance: Current disease risk-adjustment formulas in the US rely on diagnostic classification frameworks that predate the International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM). Objective: To develop an ICD-10-CM-based classification framework for predicting diverse health care payment, quality, and performance outcomes. Design Setting and Participants: Physician teams mapped all ICD-10-CM diagnoses into 3 types of diagnostic items (DXIs): main effect DXIs that specify diseases; modifiers, such as laterality, timing, and acuity; and scaled variables, such as body mass index, gestational age, and birth weight. Every diagnosis was mapped to at least 1 DXI. Stepwise and weighted least-squares estimation predicted cost and utilization outcomes, and their performance was compared with models built on (1) the Agency for Healthcare Research and Quality Clinical Classifications Software Refined (CCSR) categories, and (2) the Health and Human Services Hierarchical Condition Categories (HHS-HCC) used in the Affordable Care Act Marketplace. Each model's performance was validated using R 2, mean absolute error, the Cumming prediction measure, and comparisons of actual to predicted outcomes by spending percentiles and by diagnostic frequency. The IBM MarketScan Commercial Claims and Encounters Database, 2016 to 2018, was used, which included privately insured, full- or partial-year eligible enrollees aged 0 to 64 years in plans with medical, drug, and mental health/substance use coverage. Main Outcomes and Measures: Fourteen concurrent outcomes were predicted: overall and plan-paid health care spending (top-coded and not top-coded); enrollee out-of-pocket spending; hospital days and admissions; emergency department visits; and spending for 6 types of services. The primary outcome was annual health care spending top-coded at $250 000. Results: A total of 65 901 460 person-years were split into 90% estimation/10% validation samples (n = 6 604 259). In all, 3223 DXIs were created: 2435 main effects, 772 modifiers, and 16 scaled items. Stepwise regressions predicting annual health care spending (mean [SD], $5821 [$17 653]) selected 76% of the main effect DXIs with no evidence of overfitting. Validated R 2 was 0.589 in the DXI model, 0.539 for CCSR, and 0.428 for HHS-HCC. Use of DXIs reduced underpayment for enrollees with rare (1-in-a-million) diagnoses by 83% relative to HHS-HCCs. Conclusions: In this diagnostic modeling study, the new DXI classification system showed improved predictions over existing diagnostic classification systems for all spending and utilization outcomes considered.

Diagnosis and management of cancer risk in the gastrointestinal hamartomatous polyposis syndromes: recommendations from the U.S. Multi-Society Task Force on Colorectal Cancer.

The gastrointestinal hamartomatous polyposis syndromes are rare, autosomal dominant disorders associated with an increased risk of benign and malignant intestinal and extraintestinal tumors. They include Peutz-Jeghers syndrome, juvenile polyposis syndrome, the PTEN hamartoma tumor syndrome (including Cowden's syndrome and Bannayan-Riley-Ruvalcaba syndrome), and hereditary mixed polyposis syndrome. Diagnoses are based on clinical criteria and, in some cases, confirmed by demonstrating the presence of a germline pathogenic variant. The best understood hamartomatous polyposis syndrome is Peutz-Jeghers syndrome, caused by germline pathogenic variants in the STK11 gene. The management is focused on prevention of bleeding and mechanical obstruction of the small bowel by polyps and surveillance of organs at increased risk for cancer. Juvenile polyposis syndrome is caused by a germline pathogenic variant in either the SMAD4 or BMPR1A genes, with differing clinical courses. Patients with SMAD4 pathogenic variants may have massive gastric polyposis, which can result in gastrointestinal bleeding and/or protein-losing gastropathy. Patients with SMAD4 mutations usually have the simultaneous occurrence of hereditary hemorrhagic telangiectasia (juvenile polyposis syndrome-hereditary hemorrhagic telangiectasia overlap syndrome) that can result in epistaxis, gastrointestinal bleeding from mucocutaneous telangiectasias, and arteriovenous malformations. Germline pathogenic variants in the PTEN gene cause overlapping clinical phenotypes (known as the PTEN hamartoma tumor syndromes), including Cowden's syndrome and related disorders that are associated with an increased risk of gastrointestinal and colonic polyposis, colon cancer, and other extraintestinal manifestations and cancers. Due to the relative rarity of the hamartomatous polyposis syndromes, recommendations for management are based on few studies. This U.S. Multi-Society Task Force on Colorectal Cancer consensus statement summarizes the clinical features, assesses the current literature, and provides guidance for diagnosis, assessment, and management of patients with the hamartomatous polyposis syndromes, with a focus on endoscopic management.

Diagnosis and Management of Cancer Risk in the Gastrointestinal Hamartomatous Polyposis Syndromes: Recommendations From the US Multi-Society Task Force on Colorectal Cancer.

The gastrointestinal hamartomatous polyposis syndromes are rare, autosomal dominant disorders associated with an increased risk of benign and malignant intestinal and extraintestinal tumors. They include Peutz-Jeghers syndrome, juvenile polyposis syndrome, the PTEN hamartoma tumor syndrome (including Cowden's syndrome and Bannayan-Riley-Ruvalcaba syndrome), and hereditary mixed polyposis syndrome. Diagnoses are based on clinical criteria and, in some cases, confirmed by demonstrating the presence of a germline pathogenic variant. The best understood hamartomatous polyposis syndrome is Peutz-Jeghers syndrome, caused by germline pathogenic variants in the STK11 gene. The management is focused on prevention of bleeding and mechanical obstruction of the small bowel by polyps and surveillance of organs at increased risk for cancer. Juvenile polyposis syndrome is caused by a germline pathogenic variant in either the SMAD4 or BMPR1A genes, with differing clinical courses. Patients with SMAD4 pathogenic variants may have massive gastric polyposis, which can result in gastrointestinal bleeding and/or protein-losing gastropathy. Patients with SMAD4 mutations usually have the simultaneous occurrence of hereditary hemorrhagic telangiectasia (juvenile polyposis syndrome-hereditary hemorrhagic telangiectasia overlap syndrome) that can result in epistaxis, gastrointestinal bleeding from mucocutaneous telangiectasias, and arteriovenous malformations. Germline pathogenic variants in the PTEN gene cause overlapping clinical phenotypes (known as the PTEN hamartoma tumor syndromes), including Cowden's syndrome and related disorders that are associated with an increased risk of gastrointestinal and colonic polyposis, colon cancer, and other extraintestinal manifestations and cancers. Due to the relative rarity of the hamartomatous polyposis syndromes, recommendations for management are based on few studies. This U.S Multi-Society Task Force on Colorectal Cancer consensus statement summarizes the clinical features, assesses the current literature, and provides guidance for diagnosis, assessment, and management of patients with the hamartomatous polyposis syndromes, with a focus on endoscopic management.

Diagnosis and Management of Cancer Risk in the Gastrointestinal Hamartomatous Polyposis Syndromes: Recommendations From the US Multi-Society Task Force on Colorectal Cancer.

The gastrointestinal hamartomatous polyposis syndromes are rare, autosomal dominant disorders associated with an increased risk of benign and malignant intestinal and extraintestinal tumors. They include Peutz-Jeghers syndrome, juvenile polyposis syndrome, the PTEN hamartoma tumor syndrome (including Cowden's syndrome and Bannayan-Riley-Ruvalcaba syndrome), and hereditary mixed polyposis syndrome. Diagnoses are based on clinical criteria and, in some cases, confirmed by demonstrating the presence of a germline pathogenic variant. The best understood hamartomatous polyposis syndrome is Peutz-Jeghers syndrome, caused by germline pathogenic variants in the STK11 gene. The management is focused on prevention of bleeding and mechanical obstruction of the small bowel by polyps and surveillance of organs at increased risk for cancer. Juvenile polyposis syndrome is caused by a germline pathogenic variant in either the SMAD4 or BMPR1A genes, with differing clinical courses. Patients with SMAD4 pathogenic variants may have massive gastric polyposis, which can result in gastrointestinal bleeding and/or protein-losing gastropathy. Patients with SMAD4 mutations usually have the simultaneous occurrence of hereditary hemorrhagic telangiectasia (juvenile polyposis syndrome-hereditary hemorrhagic telangiectasia overlap syndrome) that can result in epistaxis, gastrointestinal bleeding from mucocutaneous telangiectasias, and arteriovenous malformations. Germline pathogenic variants in the PTEN gene cause overlapping clinical phenotypes (known as the PTEN hamartoma tumor syndromes), including Cowden's syndrome and related disorders that are associated with an increased risk of gastrointestinal and colonic polyposis, colon cancer, and other extraintestinal manifestations and cancers. Due to the relative rarity of the hamartomatous polyposis syndromes, recommendations for management are based on few studies. This US Multi-Society Task Force on Colorectal Cancer consensus statement summarizes the clinical features, assesses the current literature, and provides guidance for diagnosis, assessment, and management of patients with the hamartomatous polyposis syndromes, with a focus on endoscopic management.

Artificial intelligence for the assessment of bowel preparation.

BACKGROUND AND AIMS: A reliable assessment of bowel preparation is important to ensure high-quality colonoscopy. Current bowel preparation scoring systems are limited by interobserver variability. This study aimed to demonstrate objective assessment of bowel preparation adequacy using an artificial intelligence (AI)/convolutional neural network (CNN) algorithm developed from colonoscopy videos. METHODS: Two CNNs were developed using a training set of 73,304 images from 200 colonoscopies. First, a binary CNN was developed and trained to distinguish video frames that were appropriate versus inappropriate for scoring with the Boston Bowel Preparation Scale (BBPS). A second multiclass CNN was developed and trained on 26,950 appropriate frames that were expertly annotated with BBPS segment scores (0-3). We validated the algorithm using 252 10-second video clips that were assigned BBPS segment scores by 2 experts. The algorithm provided mean BBPS scores based on the algorithm (AI-BBPS) by calculating mean BBPS based on each frame's scoring. We maximized the algorithm's performance by choosing a dichotomized AI-BBPS score that closely matched dichotomized BBPS scores (ie, adequate vs inadequate). We tested the mean BBPS score based on the algorithm AI-BBPS against human rating using 30 independent 10-second video clips (test set 1) and 10 full withdrawal colonoscopy videos (test set 2). RESULTS: In the validation set, the algorithm demonstrated an area under the curve of .918 and accuracy of 85.3% for detection of inadequate bowel cleanliness. In test set 1, sensitivity for inadequate bowel preparation was 100% and agreement between raters and AI was 76.7% to 83.3%. In test set 2, sensitivity for inadequate bowel preparation for each segment was 100% and agreement between raters and AI was 68.9% to 89.7%. Agreement between raters alone versus raters and AI were similar (κ = .694 and .649, respectively). CONCLUSIONS: The algorithm assessment of bowel cleanliness as measured with the BBPS showed good performance and agreement with experts including full withdrawal colonoscopies.

Updates on Age to Start and Stop Colorectal Cancer Screening: Recommendations From the U.S. Multi-Society Task Force on Colorectal Cancer.

This document is a focused update to the 2017 colorectal cancer (CRC) screening recommendations from the U.S. Multi-Society Task Force on Colorectal Cancer, which represents the American College of Gastroenterology, the American Gastroenterological Association, and the American Society for Gastrointestinal Endoscopy. This update is restricted to addressing the age to start and stop CRC screening in average-risk individuals and the recommended screening modalities. Although there is no literature demonstrating that CRC screening in individuals under age 50 improves health outcomes such as CRC incidence or CRC-related mortality, sufficient data support the U.S. Multi-Society Task Force to suggest average-risk CRC screening begin at age 45. This recommendation is based on the increasing disease burden among individuals under age 50, emerging data that the prevalence of advanced colorectal neoplasia in individuals ages 45 to 49 approaches rates in individuals 50 to 59, and modeling studies that demonstrate the benefits of screening outweigh the potential harms and costs. For individuals ages 76 to 85, the decision to start or continue screening should be individualized and based on prior screening history, life expectancy, CRC risk, and personal preference. Screening is not recommended after age 85.

Updates on age to start and stop colorectal cancer screening: recommendations from the U.S. Multi-Society Task Force on Colorectal Cancer.

This document is a focused update to the 2017 colorectal cancer (CRC) screening recommendations from the U.S. Multi-Society Task Force on Colorectal Cancer, which represents the American College of Gastroenterology, the American Gastroenterological Association, and the American Society for Gastrointestinal Endoscopy. This update is restricted to addressing the age to start and stop CRC screening in average-risk individuals and the recommended screening modalities. Although there is no literature demonstrating that CRC screening in individuals under age 50 improves health outcomes such as CRC incidence or CRC-related mortality, sufficient data support the U.S. Multi-Society Task Force to suggest average-risk CRC screening begin at age 45. This recommendation is based on the increasing disease burden among individuals under age 50, emerging data that the prevalence of advanced colorectal neoplasia in individuals ages 45 to 49 approaches rates in individuals 50 to 59, and modeling studies that demonstrate the benefits of screening outweigh the potential harms and costs. For individuals ages 76 to 85, the decision to start or continue screening should be individualized and based on prior screening history, life expectancy, CRC risk, and personal preference. Screening is not recommended after age 85.

Updates on Age to Start and Stop Colorectal Cancer Screening: Recommendations From the U.S. Multi-Society Task Force on Colorectal Cancer.

This document is a focused update to the 2017 colorectal cancer (CRC) screening recommendations from the U.S. Multi-Society Task Force on Colorectal Cancer, which represents the American College of Gastroenterology, the American Gastroenterological Association, and the American Society for Gastrointestinal Endoscopy. This update is restricted to addressing the age to start and stop CRC screening in average-risk individuals and the recommended screening modalities. Although there is no literature demonstrating that CRC screening in individuals under age 50 improves health outcomes such as CRC incidence or CRC-related mortality, sufficient data support the U.S. Multi-Society Task Force to suggest average-risk CRC screening begin at age 45. This recommendation is based on the increasing disease burden among individuals under age 50, emerging data that the prevalence of advanced colorectal neoplasia in individuals ages 45 to 49 approaches rates in individuals 50 to 59, and modeling studies that demonstrate the benefits of screening outweigh the potential harms and costs. For individuals ages 76 to 85, the decision to start or continue screening should be individualized and based on prior screening history, life expectancy, CRC risk, and personal preference. Screening is not recommended after age 85.