Edelweiss Publications

New Insights on Covid-19 Treatment 🧐

SARS-CoV-2 Infection is Protease-Dependent and Induces Neutrophils “Proteolytic Storm” Triggering Clinical Worsening and Viral Sepsis. Proteolysis and Inhibitors of Neutrophil Release Can Prevent and Treat Covid-19

https://www.linkedin.com/pulse/sars-cov-2-infection-protease-dependent-induces-storm-taha-nafees-1c/?published=t

SARS-CoV-2 Infection is Protease-Dependent and Induces Neutrophils “Proteolytic Storm” Triggering Clinical Worsening and Viral Sepsis. Proteolysis and Author (s): Pier Maria Fornasari Free access links to article: PDF link: http://edelweisspublications.com/edelweiss/article/sars-cov-infection-protease-dependent-induces-neutrophils-proteolytic.

https://www.linkedin.com/pulse/urinary-c-peptide-excretion-diabetic-treatment-low-diet-vidya-gouru/?published=t

New Article:
Management of Metabolic Acidosis in the Post-Cardiac Surgical Patient
By Jeevan Francis, et al.

Full free Access: http://edelweisspublications.com/articles/37/687/management-metabolic-acidosis-post-cardiac-surgical-patient

Abstract
The base deficit is the best way to evaluate severity of Metabolic Acidosis (MA). It indicates a value corresponding to the number of mmol/L below 24 of the measured bicarbonate concentration. Base deficit between 0 and 5 mmol/L indicates that the patient is not at risk of immediate harm. Arterial blood gases are typically measured every 2-4 hours following cardiac surgery and there is always a trend in base deficit changes to consider. Where the base deficit is diminishing, this indicates that the patient is improving, whereas when it is worsening, the opposite is true. Base deficits between 5 and 10 indicate that a serious problem is present which requires urgent correction. Where the base deficit is greater than 10, cardiac arrest may occur, and such patients require constant supervision by a doctor if active management is being pursued. Where the base deficit is persistently greater than 15, survival is extremely unlikely. This degree of acidosis is associated with widespread disruption of mitochondria at cellular level. The mitochondria often do not recover even if the precipitating cause of the MA is corrected, in which case the patient develops fatal multisystem organ failure. The management of MA in post-cardiac surgical patients is indivisibly bound up in optimizing circulatory physiology. We have not expounded on how this foundational knowledge should be applied but without it the management of MA in this patient population will be severely hampered.