COVID-19’da Koagülopati

Yazarlar

Hediye Çiğdem Şimşek
https://orcid.org/0000-0003-1615-1164

Özet

COVID-19 enfeksiyonunda koagülopati ve tromboembolik olaylar, hastalığın ciddiyeti, klinik seyri ve kötü prognozu ile doğrudan ilişkili temel karakteristik özelliklerdir. Virüsün yol açtığı kontrolsüz sitokin fırtınası; vasküler endotel hasarına, doku faktörü ekspresyonuna, kompleman aktivasyonuna, trombosit ile lökosit aktivasyonuna ve doğal antikoagülan mekanizmaların bozulmasına neden olarak pulmoner mikrotrombüs ve sistemik tromboz riskini belirgin şekilde artırır. Akciğer vaskülatüründe lokalize olan bu immün-enflamatuvar ve hemostatik bozukluklar, hipoksi, ARDS ve çoklu organ yetmezliği tablosunu şiddetlendirir. Şiddetli COVID-19 hastalarında D-dimer düzeylerindeki aşırı yükselme, protrombin zamanı (PT) uzaması, trombositopeni ve hastalığın ilerleyen evrelerinde ortaya çıkabilen hipofibrinojenemi, yoğun bakım ihtiyacı ve yüksek hastane içi mortalite ile güçlü bir şekilde ilişkilendirilmiştir. COVID-19 ilişkili koagülopati; belirgin bir tüketim koagülopatisi tablosu sunmaması, ciddi kanama olaylarının nadir görülmesi ve sistemik DIC'ten çok pulmoner intravasküler koagülasyona işaret etmesiyle klasik DIC, trombotik mikroanjiyopati ve hemofagositik lenfohistiyositoz sendromlarından farklılık gösterir. Tedavide düşük molekül ağırlıklı heparin (DMAH) kullanımıyla tromboprofilaksi önerilmekte; heparinin pıhtılaşmayı önleyici etkisinin yanı sıra virüsün diken proteinine bağlanarak hücreye girişini engellediği, mortaliteyi ve pulmoner koagülopatiyi azalttığı bildirilmektedir. Bununla birlikte, olası gastrointestinal kanama ve heparine bağlı trombositopeni riskleri göz önünde bulundurularak D-dimer, PT, APTT, trombosit ve fibrinojen parametrelerinin dinamik olarak takip edilmesi ve tedavinin patofizyolojik duruma göre optimize edilmesi tavsiye edilir.

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Yayınlanan

10 Mayıs 2021

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