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Background and study aims Esophageal defects (leaks, fistulas, and perforations) are associated with significant morbidity and mortality. Endoluminal vacuum-assisted closure (EVAC) is a novel intervention that entails the use of sponges in the defect along with negative pressure to achieve granulation tissue formation and healing and has been gaining popularity. We performed a systematic review and pooled analysis of available literature to assess the safety and effectiveness of EVAC for esophageal defects. Patients and methods We queried PubMed/Medline, Embase, Cochrane, and Web of Science through September 25, 2020 to include all pertinent articles highlighting the safety and effectiveness profile of EVAC for esophageal defects. Pooled rates, 95 % confidence intervals (CIs), and heterogeneity (I2 ) were assessed for each outcome. Results A total of 18 studies with 423 patients were included (mean age 64.3 years and males 74.4 %). The technical success for EVAC was 97.1 % (CI: 95.4 %–98.7 %, I2  = 0 %). The clinical success was 89.4 % (CI: 85.6 %–93.1 %, I2  = 36.8 %). The overall all-cause mortality and adverse events (AEs) noted were 7.1 % (CI: 4.7 %–9.5 %, I2  = 0 %) and 13.6 % (CI: 8.0 %–19.1 %, I2  = 68.9 %), respectively. The pooled need for adjuvant therapy was 15.7 % (CI: 9.8 %–21.6 %, I2  = 71.1 %). Conclusions This systematic review and meta-analysis showed high rates of technical success, clinical success, and low all-cause mortality and AEs using EVAC. Although the technique is a promising alternative, the lack of comparative studies poses a challenge in making definite conclusions regarding use of EVAC compared to other endoscopic modalities, such as clips and stents.

Background Recently, amongst other hemostatic modalities, Hemospray (TC-325) has emerged as an effective method for managing patients with non-variceal upper gastrointestinal bleeding (GIB). We conducted this systematic review and meta-analysis to assess the efficacy of Hemospray in patients with non-variceal upper GIB. Methods Our primary outcomes were clinical and technical success; secondary outcomes were aggregate rebleeding, early rebleeding, delayed rebleeding, refractory bleeding, mortality, and treatment failure. A meta-analysis of proportions was conducted for all reported primary and secondary outcomes. A relative risk meta-analysis was conducted for studies reporting direct comparisons between Hemospray and other hemostatic measures. Results A total of 20 studies with 1280 patients were included in the final analysis. Technical success of Hemospray was seen in 97% of cases (95% confidence interval [CI] 94-98%, I 2 =52.89%) and a significant trend towards increasing technical success was seen during publication years 2011-2019. Clinical success of Hemospray was seen in 91% of cases (95%CI 88-94%, I 2 =47.72%), compared to 87% (95%CI 75-94%, I 2 =0.00%) for other hemostatic measures. The secondary outcomes of aggregate rebleeding, early rebleeding, delayed rebleeding, refractory rebleeding, mortality and treatment failure following the use of Hemospray were seen in 27%, 20%, 9%, 8%, 8%, and 31% of cases, respectively. Conclusion Hemospray is safe, effective and non-inferior to traditional hemostatic measures for the management of non-variceal upper GIB, and can thus be used as an alternative option.

Dieulafoy's lesion is an abnormally large, tortuous, submucosal vessel that erodes the overlying mucosa, without primary ulceration or erosion. Although these lesions predominantly involve the stomach and upper small intestine, they are being detected with increasing frequency in the rectum. We conducted a systematic literature search of MEDLINE, Cochrane, Embase, and Scopus databases for adult rectal Dieulafoy's lesion. After careful review of the search results, a total of 101 cases were identified. The data on patient characteristics, clinical features, colonoscopy findings, diagnosis, treatment, and clinical outcomes were collected and analyzed. The mean age of presentation was 66±17 years (range, 18-94 years), with 54% of cases reported in males. Clinical presentation was dominated by acute lower gastrointestinal bleeding in the form of bright-red blood per rectum 47% and hematochezia 36%, whereas 16% of patients were admitted with symptoms related to other medical conditions. Major underlying disorders were hypertension 29%, diabetes mellitus 21%, and chronic kidney disease 16%. The average number of colonoscopies required for the diagnosis of rectal Dieulafoy's lesion was 1.5±0.7. In regard to treatment, endoscopic therapy was applied in 80%, direct surgical suturing in 12%, angiographic embolization in 4%, and endoscopic therapy followed by surgical ligation was performed in 4% of patients. The endoscopic treatment was a feasible choice for rectal disease, with a primary hemostasis rate of 88%. Although the overall mortality rate was 6%, the causes of death were unrelated to this entity. This review illustrates that patients with rectal Dieulafoy's lesion can have a favorable clinical outcome. Prompt diagnosis and appropriate management are of paramount importance to prevent serious hemodynamic complications. The best therapeutic modality remains to be determined but the data presented here support the use of mechanical endoscopic methods as safe and effective.

Despite extensive research in the pathogenesis, early detection, and therapeutic approaches of pancreatic ductal adenocarcinoma (PDAC), it remains a devastating and incurable disease. As the global incidence and prevalence of PDAC continue to rise, there is a pressing need to place strong emphasis on its prevention. Although it is widely recognized that cigarette smoking, a potentially modifiable risk factor, has been linked to PDAC development, its contribution to prognosis is still uncertain. Moreover, the mechanistic pathways of PDAC progression secondary to smoking are various and lack a summative narration. Herein, we update and summarize the direct and indirect roles cigarette smoking plays on PDAC development, review literature to conclude the impact cigarette smoking has on prognosis, and postulate a comprehensive mechanism for cigarette smoking-induced PDAC.