COVID-19-associated coagulopathy in children and adolescents (literature review)

The pandemic of the new coronavirus infection COVID-19 in 2020 has become the main health problem across the globe. A special characteristic of the SARS-CoV-2 virus is tropism to the vascular endothelium with the development of endotheliitis, which entails a number of typical disorders of the blood coagulation system: coagulopathy with increased thrombin generation, D-dimer, decreased fibrinolysis and prolonged prothrombin time. The coagulation disorder in COVID-19 is called thromboinflammation. Hyperinflammation, increased blood levels of von Willebrand factor, coagulation factor VIII, neutrophil extracellular traps, platelet activation, microvesicles play a significant role in the pathogenesis of hypercoagulation in COVID-19. To date, it is known that cases of COVID-19 in children and adolescents constitute a small part of the total number of patients with diagnosed COVID-19, and disorders of the blood coagulation system are similar to those in adults. The degree of hypercoagulable syndrome and the risk of thrombosis depend on the severity of COVID-19. And for children they are most expressed with the development of a hyperinflammatory immune response, called multisystem inflammatory syndrome. At the same time, clinical studies of the pathogenesis of COVID-19 in adults and children and the search for optimal methods of therapy for thrombus inflammation, which underlies the pathogenesis of COVID-19, continue. © 2021 Novosibirsk State University. All rights reserved.

Kawasaki disease and multisystem inflammatory syndrome in children with COVID-19 infection

During the COVD-19 pandemic, some pediatric patients in many countries around the world experienced a syndrome resembling a severe Kawasaki disease (KD), often accompanied by shock. Due to the incomplete signs of the classic KD in the era before the present pandemic, in many publications from European countries and the United States, this condition was called «multisystem inflammatory syndrome in children - MIS-C» or «hyperinflammatory shock» or «Kawasaki-like syndrome». This syndrome with a new coronavirus infection is characterized by refractory fever, frequent gastrointestinal symptoms, heart damage (including coronary dilation in some patients, and acute left ventricular failure in the majority), increased ESR and CRP levels, neutrophilia, extremely high troponin levels, increased ferritin, AST, ALT, lactate dehydrogenase, creatine phosphate kinase, interleukin-6 and interleukin-10, coagulopathy with an increase in D-dimer and fibrinogen, thrombocytopenia, sometimes procalcitonin increase. The manifestations of a cytokine storm may meet the criteria for secondary hemophagocytic syndrome. The mechanism of myocardial damage remains unclear. Treatment with high-dose intravenous immunoglobulin is effective, and in the presence of signs of hemophagocytic syndrome, dexamethasone or methylprednisolone. Further research is needed to understand the pathogenesis, resemblance and differences of this syndrome with classic KD, understanding of heart injuiry and early recognition for the need of urgent care. В ходе пандемии COVD-19 у части пациентов детского возраста во многих странах мира отмечен синдром, напоминающий тяжелый вариант болезни Кавасаки (БК), часто сопровождаемый шоком. Ввиду неполного его соответствия классической БК в эру до настоящей пандемии во многих публикациях из европейских стран и США это состояние получило название «мультисистемный воспалительный синдром», либо «гипервоспалительный шок», либо «Кавасаки-подобный синдром». Для данного синдрома при новой коронавирусной инфекции характерны рефрактерная лихорадка, частые гастроинтестинальные симптомы, поражение сердца (включая коронарную дилатацию у части больных и острую левожелудочковую недостаточность у большинства), повышение уровня СОЭ и СРБ, нейтрофилез, экстремально высокий уровень тропонина, рост ферритина, АСТ, АЛТ, лактатдегидрогеназы, креатинфосфаткиназы, интерлейкина-6 и интерлейкина-10, коагулопатия с увеличением Д-димера и фибриногена, тромбоцитопения, иногда рост прокальцитонина. Проявления цитокинового шторма могут отвечать критериям вторичного гемофагоцитарного синдрома (ГФС). Механизм поражения миокарда остается неясным. Эффективно лечение высокодозным внутривенным иммуноглобулином, при наличии признаков ГФС - дексаметазоном либо метилпреднизолоном. Дальнейшие исследования необходимы для понимания патогенеза, сходства и различия данного синдрома с классической БК, механизма поражения сердца, раннего распознавания для оказания ургентной помощи.