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Marcel Vetter1 12 2, Timo Rath1 12 2, Jürgen Siebler1 12 2, Maximilian Waldner1 12 2, Markus F Neurath1 12 2, Lukas Pfeifer3 3 1Department of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany; 2Deutsches Zentrum Immuntherapie, DZI, Erlangen, Germany; 3Department of Gastroenterology and Interventional Endoscopy, Krankenhaus Barmherzige Brüder, Regensburg, GermanyCorrespondence: Lukas PfeiferDepartment of Gastroenterology and Interventional Endoscopy, Krankenhaus Barmherzige Brüder, Prüfeninger Straße 86, Regensburg, Bavaria, 93049, GermanyTel +49 941 369 2051Fax +49 941 369 2055Email Lukas.Pfeifer@barmherzige-regensburg.deBackground: Ingestion of alkaline fluids is a common problem, which can lead to perforations, strictures and malignancy. We present a rare case series of several patients who accidentally ingested the same alkaline substance in different doses.Methods: We investigated four patients with accidental ingestion of dishwashing liquid. All patients underwent gastroscopy within 24h after inpatient admission. Gastroesophageal lesions were classified according to the Zargar classification for corrosive ingestions.Results: Esophagogastric lesions were predominantly found at the distal esophagus and the small curvature of the stomach. The severity of these lesions ranged from mild erosions (Zargar 2A) to marked necrosis (Zargar 3A). Our data suggest that the degree of these lesions correlated with the amount of ingested toxin and duration of the inpatient stay. However, a low symptom severity or inconspicuous otolaryngologic examination did not exclude severe gastroesophageal lesions.Conclusion: Our data suggest that the severity of gastroesophageal lesions correlates with the amount of ingested alkaline substance. Symptom burden and an otolaryngologic examination are not sufficiently predictive for the severity of gastroesophageal lesions. The composition and quantity of the swallowed liquid should be determined.Keywords: alkali ingestion, gastroscopy, toxin dose, case series

Introduction: Cardiopulmonary bypass is an essential component of cardiothoracic surgeries. However, significant complications such as systemic inflammatory response syndrome (SIRS) resulting from cardiopulmonary bypass (CPB) are a common occurrence due to contact between circulating blood and foreign surfaces that leads to platelet activation. It is suggested that different available CPB circuit coatings can potentially reduce platelet activation. However, there have been no published evidence-based reports confirming these claims. In addition, there is no well-established protocol for studying platelet activation biomarkers during CPB in vitro in a laboratory setting. Methods: CPB was simulated in the laboratory using bovine blood in two different types of coated CPB circuits: Trillium® Biosurface by Medtronic, and XcoatingTM Surface by Terumo. Fresh bovine blood samples were collected and circulated through the CPB circuit following the standard protocol used in the operation rooms. Blood samples were then collected at 5 min, 30 min, and 55 min during the circulation. Blood plasmas were separated and subjected to enzyme-linked immunosorbent assay to measure most established platelet activation markers P-selectin, Platelet Factor 4 (PF4), Glycoprotein IIb/IIIa (GPIIb/IIIa), and β-thromboglobulin (β-TG) at different time points. Results: The biomarker values at 30 min and 55 min were compared to the base values at 5 min for each type of CPB circuit. The results of the means from all measured biomarkers showed data measurements that indicated no significant variability within each coating. All collected data points fell within ±2 SD of the means, which was considered acceptable variations across technical replicates. Conclusion: In this study, we were able to establish an in vitro protocol in the laboratory setting that is precise and reliable with minimum intra-variability. This established protocol will allow for future studies in which different coated CPB circuits can be compared for their effectiveness in blocking platelet activation during the CPB.