COVID-19, septic shock and syndrome of disseminated intravascular coagulation syndrome. Part 1

The pandemic of a new coronavirus infection (Coronavirus Disease 2019, COVID-19) caused by SARS-CoV-2 became a real challenge to humanity and the medical community in 2020 and raised a number of medical, social and even philosophical questions. An almost avalanche-like increase in the number of infected people in a short time, due to the high contagiousness of viral infection, allowed us to identify groups of patients with mild, moderate and severe forms of the disease. Doctors around the world are faced with an acute problem of treating a large number of patients in critical conditions caused by COVID-19. From the currently available information on clinical cases of COVID-19, it follows that COVID-19 patients in critical condition have a clinical picture of disseminated intravascular coagulation (DIC), septic shock with the development of multiple organ failure. The first part of the article discusses the pathogenesis of non-specific universal biological responses of the body in critical condition ― from the Sanarelli-Schwartzman phenomenon to the DIC, septic shock, systemic inflammatory response syndrome and the so-called neutrophil extracellular traps (NETs). The questions of cytokine storm in severe forms of systemic inflammatory response syndrome (SIRS), the role of inflammation in the activation of coagulation, and the relationship between inflammation and thrombosis are discussed. Modern ideas about the mechanisms of so-called NETosis, their role in the occurrence of immunothrombosis and inflammation-induced thrombosis in autoimmune diseases ― vasculitis, antiphospholipid syndrome, and systemic lupus erythematosus is highlighted. The article discusses the possibility of participation of ADAMTS-13 metalloproteinase in the pathogenesis of multiple organ failure in severe endotheliopathy in patients with viral septic shock

Administration of antenatal corticosteroid is associated with reduced fetal growth velocity: a longitudinal study

To elucidate whether antenatal administration of corticosteroids in pregnancies with threatened preterm labor affects growth velocity

Cardiac function in fetal growth restriction: a review

Fetal growth restriction (FGR) is defined as the inability of the fetus to reach its growth potential. According to the onset of the disease is defined early (< 32 weeks) or late (≥ 32 weeks). FGR is associated with an increased risk of adverse short- and long-term outcomes, including hypoxemic events and neurodevelopmental delay compared to normally grown fetuses and increased risk of complications in the infanthood and adulthood. The underlying cause of FGR is placental insufficiency leading to chronic fetal hypoxia that affects cardiac hemodynamic with different mechanism in early and late onset growth restriction. In early onset FGR adaptive mechanisms involve the diversion of the cardiac output preferentially in favour of the brain and the heart, while abnormal arterial and venous flow manifest in the case of further worsening of fetal hypoxia. In late FGR the fetal heart shows a remodelling of its shape and function mainly related to a reduction of umbilical vein flow. In this review we discuss the modifications occurring at the level of the fetal cardiac hemodynamic in fetuses with early and late FGR