Коагулопатия при COVID-19

Нарушения гемостаза играют важную роль в патогенезе и клинических проявлениях COVID-19. Целью работы явилось подробное рассмотрение патогенеза, клинических проявлений, методов диагностики и лечения коронавирус-индуцированной коагулопатии (КИК). При дебюте COVID-19 выявляется гиперкоагуляция, а коагулопатия потребления, синдром диссеминированного внутрисосудистого свертывания (ДВС) регистрируются обычно на поздних стадиях заболевания. В патогенезе гиперкоагуляции при COVID-19 играют роль провоспалительные цитокины, гиперфибриногенемия, повышенное содержание в крови фактора Виллебранда, фактора VIII, нейтрофильных внеклеточных ловушек, активация тромбоцитов, выработка антифосфолипидных антител, микровезикулы. В лабораторных показателях выявляются повышенные плазменные концентрации D-димера, фибриногена, увеличение протромбинового времени и уменьшение количества тромбоцитов. Кумулятивная частота тромботических осложнений колеблется от 21 до 31 %. Факторами риска тромбозов являются пребывание в отделении интенсивной терапии, лейкоцитоз и высокая концентрация D-димера в плазме. Дифференциальный диагноз КИК следует проводить с ДВС-синдромом, сепсис-индуцированной коагулопатией, антифосфолипидным, гемофагоцитарным синдромами, тромботической микроангиопатией, гепарин-индуцированной тромоцитопенией. Возможно сочетание КИК с сепсисом, антифосфолипидным синдромом, гемофагоцитарным синдромом, тромботической микроангиопатией, гепарин-индуцированной тромбоцитопенией.

Основной терапией является лечение низкомолекулярными гепаринами. Приводятся рекомендации по лечению.

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