Complicaciones trombóticas en COVID-19: un recuento en la fisiopatología, alteraciones hematológicas, diagnóstico y tratamiento.
Resumen
La enfermedad por coronavirus (COVID‑19) es provocada por el coronavirus tipo 2 causante del síndrome respiratorio agudo severo (SARS-CoV-2) que afecta múltiples órganos. Se caracteriza por una tormenta de citoquinas que desencadena inflamación, disfunción endotelial, trombosis micro y macrovascular, que pueden dañar otros órganos además del pulmón. De un 20 a 50% de los pacientes en servicio de hospitalización por enfermedad grave causada por el COVID-19 presentan alteraciones hematológicas en las pruebas de coagulación. Se llevó a cabo una búsqueda en bases de datos como PubMed, Lilacs, ScienceDirect, Scielo y Redalyc, con diferentes combinaciones de palabras claves y términos MESH como: Coronavirus Infections, Thrombosis, Angiotensin II, Hemostasis posteriormente se realizó un análisis y resumen de la información revisada. Dentro de los laboratorios alterados se destaca: un dímero D elevado, tiempo parcial de tromboplastina (TPT) y tiempo de protrombina (TP) prolongados, niveles disminuidos de fibrinógeno y trombocitopenia leve, estos resultados se asocian a una mayor incidencia de eventos trombóticos como el tromboembolismo venoso (TEV) y un mayor riesgo de muerte para el paciente. El virus SARS-COV-2 altera significativamente el sistema hematológico, exacerbando la respuesta inmune, lesión endotelial, lo que lleva a un estado trombótico debido a la estancia hospitalaria. El diagnóstico de este estado se establece mediante estudios de laboratorio como marcadores de inflamación (proteína C reactiva, eritrosedimentación y recuento plaquetario), pruebas de coagulación e imágenes diagnósticas, de estos dependen la clasificación del riesgo y el posterior esquema terapéutico.
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Derechos de autor 2024 Miguel Eduardo Saavedra-Valencia, Lina Maria Martinez-Sanchez, Marielena Fonseca-Guzmán
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