Percutaneous endoscopic necrosectomy (PEN) for treatment of necrotizing pancreatitis: a systematic review and meta-analysis.

Background and study aims Endoscopic necrosectomy is limited by the proximity of necrosis to the gastrointestinal tract. Percutaneous endoscopic necrosectomy (PEN) is a minimally invasive endoscopic method of percutaneous debridement. Studies regarding its efficacy and safety are lacking. The purpose of this study was to assess the efficacy and safety of PEN in necrotizing pancreatitis. Methods Pubmed, Ovid, Cochrane, Scopus and Web of Science Database were searched from inception through February 2021. Dual extraction and quality assessment of studies using Cochrane risk of bias tool were performed independently by two authors. The primary outcome was defined as clinical success of PEN. Secondary outcomes included periprocedural morbidity, mortality, and long-term morbidity and mortality. Results Sixteen observational studies including 282 subjects were analyzed. The average reported age of the participants was 50.3 years. Patients with reported gender included 39 % females and 61 % males. The success rate as defined by complete resolution of necrosis and removal of drainage catheters/stents was 82 % (95 % confidence interval 77-87). The mean size of pancreatic necrosis was 14.86 cm (5-54 cm). The periprocedural morbidity rate was 10 %, while there was no reported periprocedural mortality. The long-term morbidity rate was reported as 23 % and mortality at follow-up was 16 %. Conclusions PEN is a novel method of endoscopic management of pancreatic necrosis. Based on our meta-analysis of retrospective studies, it represents a safe treatment modality with high rates of clinical success and low rates of perioperative morbidity and mortality. This study supports the use of PEN when conventional endoscopic therapy is not feasible.

An outpatient telehealth elective for displaced clinical learners during the COVID-19 pandemic.

BACKGROUND: In response to the COVID-19 pandemic, medical schools suspended clinical rotations. This displacement of medical students from wards has limited experiential learning. Concurrently, outpatient practices are experiencing reduced volumes of in-person visits and are shifting towards virtual healthcare, a transition that comes with its own logistical challenges. This article describes a workflow that enabled medical students to engage in meaningful clinical education while helping an institution's outpatient practices implement remote telemedicine visits. METHODS: A 4-week virtual elective was designed to allow clinical learners to participate in virtual telemedicine patient encounters. Students were prepared with EMR training and introduced to a novel workflow that supported healthcare providers in the outpatient setting. Patients were consented to telehealth services before encounters with medical students. All collected clinical information was documented in the EMR, after which students transitioned patients to a virtual Doxy.me video appointment. Surveys were used to evaluate clinical and educational outcomes of students' participation. Elective evaluations and student reflections were also collected. RESULTS: Survey results showed students felt well-prepared to initiate patient encounters. They expressed comfort while engaging with patients virtually during telemedicine appointments. Students identified clinical educational value, citing opportunities to develop patient management plans consistent with in-person experiences. A significant healthcare burden was also alleviated by student involvement. Over 1000 total scheduled appointments were serviced by students who transitioned more than 80 % of patients into virtual attending provider waiting rooms. CONCLUSIONS: After piloting this elective with fourth-year students, pre-clerkship students were also recruited to act in a role normally associated with clinical learners (e.g., elicit patient histories, conduct a review of systems, etc.). Furthermore, additional telemedicine electives are being designed so medical students can contribute to patient care without risk of exposure to COVID-19. These efforts will allow students to continue with their clinical education during the pandemic. Medical educators can adopt a similar workflow to suit evolving remote learning needs.

The impact of acute kidney injury on mortality and clinical outcomes in patients with alcoholic cirrhosis in the USA.

INTRODUCTION: Acute kidney injury (AKI) is associated with increased morbidity and mortality in patients with chronic liver disease. Although the impact of AKI on patients with liver disease has been established, its impact on alcoholic cirrhosis has not been studied. METHODS: Our study utilized data from the National Inpatient Sample for the year 2016 for all patients with a diagnosis of alcoholic cirrhosis and AKI. Primary outcomes were mortality, length of stay (LOS) and hospitalization cost were compared. Secondary outcomes were complications of cirrhosis and its impact on mortality. Multivariate logistic regression analysis and propensity-score matching were used to compare the two groups. RESULTS: A total of 29 906 patients were included and 6733 (22.5%) had AKI. Propensity-matched multivariate analysis demonstrates that AKI was associated with a significant increase risk of mortality [odds ratio (OR): 8.09; 95% confidence interval (CI), 6.68-9.79; P < 0.0001]. AKI prolonged the hospital stay by 3.68 days (95% CI, 3.42-3.93; P < 0.0001) and increased total hospital charges by $50 284 (95% CI, 45 829-54 739; P < 0.0001). AKI increased the risk of complications of cirrhosis, including hepatorenal syndrome (OR: 19.15; 95% CI, 16.1-22.76), ascites (OR: 2.27; 95% CI, 2.11-2.44), hepatic encephalopathy (OR: 2.54; 95% CI, 1.87-3.47) and portal hypertension (OR: 1.08; 95% CI, 1.01-1.16). CONCLUSION: AKI in alcoholic cirrhosis significantly increases the risk of mortality, hospitalizations costs and LOS. Further studies are needed on addressing renal failure and treatment options for patients with alcoholic cirrhosis.

Barrett's metaplasia develops from cellular reprograming of esophageal squamous epithelium due to gastroesophageal reflux.

Gastroesophageal reflux disease (GERD) clinically predisposes to columnar Barrett's metaplasia (BM) in the distal esophagus. We demonstrate evidence supporting the cellular origin of BM from reprograming or transcommitment of resident normal esophageal squamous (NES) epithelial cells in response to acid and bile (A + B) exposure using an in vitro cell culture model. The hTERT-immortalized NES cell line NES-B10T was exposed 5 min/day to an A + B mixture for 30 wk. Morphological changes, mRNA, and protein expression levels for the inflammatory marker cyclooxygenase-2; the lineage-determining transcription factors TAp63 (squamous), CDX2, and SOX9 (both columnar); and the columnar lineage markers Villin, Muc-2, CK8, and mAb Das-1 (incomplete phenotype of intestinal metaplasia) were assessed every 10 wk. Markers of columnar lineage and inflammation increased progressively, while squamous lineage-determining transcriptional factors were significantly decreased both at the mRNA and/or protein level in the NES-B10T cells at/after A + B treatment for 30 wk. Distinct modifications in morphological features were only observed at/after 30 wk of A + B exposure. These changes acquired by the NES-B10T 30-wk cells were retained even after cessation of A + B exposure for at least 3 wk. This study provides evidence that chronic exposure to the physiological components of gastric refluxate leads to repression of the discernable squamous transcriptional factors and activation of latent columnar transcriptional factors. This reflects the alteration in lineage commitment of the precursor-like biphenotypic, NES-B10T cells in response to A + B exposure as the possible origin of BM from the resident NES cells.NEW & NOTEWORTHY This study provides evidence of the origins of Barrett's metaplasia from lineage transcommitment of resident esophageal cells after chronic exposure to gastroesophageal refluxate. The preterminal progenitor-like squamous cells alter their differentiation and develop biphenotypic characteristics, expressing markers of incomplete-type columnar metaplasia. Development of these biphenotypic precursors in vitro is a unique model to study pathogenesis of Barrett's metaplasia and esophageal adenocarcinoma.