Tromboembolismo pulmonar y COVID-19: un cambio de paradigma

Franco-Moreno, Ana Isabel; Muñoz‐Rivas, Nuria; Mestre-Gómez, B.; Torres‐Macho, Juan

doi:10.1016/j.rce.2020.05.006

Cited by 7 publications

(5 citation statements)

References 14 publications

(9 reference statements)

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“…9 This points to the possibility that local lung inflammation and pulmonary microthrombosis are especially prominent in COVID-19. 11 Similar findings have been observed in our study, with a higher proportion of patients with PE alone (1.4%) than DVT alone (0.4%) or in combination (0.2%). These data suggest that the use of tests specifically for detecting DVT is not sufficient for detecting VTE in COVID-19.…”

Section: Discussionsupporting

confidence: 92%

“…[1][2][3] VTE has been detected in 3 to 46% of the patients with COVID-19, with the highest prevalence in patients in intensive care units (ICU). [4][5][6][7][8][9][10][11][12][13][14][15][16][17] These rates are higher than those reported in non-COVID-19 patients [18][19][20] and have been related to a higher mortality. 5 The diagnosis of VTE in patients with COVID-19 is challenging because its clinical manifestations and analytical findings can be misdiagnosed.…”

Section: Introductionmentioning

confidence: 69%

See 1 more Smart Citation

Estimation of Admission D-dimer Cut-off Value to Predict Venous Thrombotic Events in Hospitalized COVID-19 Patients: Analysis of the SEMI-COVID-19 Registry

et al. 2021

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 69%

Estimation of Admission D-dimer Cut-off Value to Predict Venous Thrombotic Events in Hospitalized COVID-19 Patients: Analysis of the SEMI-COVID-19 Registry

et al. 2021

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“…El SARS-CoV-2 infecta las células endoteliales que expresan ACE2 (enzima convertidora de angiotensina II). Este daño endotelial activa el factor tisular, que genera trombina a partir de protrombina por acción del factor X activado; las plaquetas circulantes activadas se agregan y proporcionan la superficie fosfolipídica adecuada para la adhesión de los diferentes compuestos de la cascada de la coagulación así como activación del complemento, con formación de C3a y C5a, capaces de reclutar neutrófilos, macrófagos, linfocitos y monocitos, responsables de la liberación masiva de citoquinas proinflamatorias (IL-1, IL-6, IL-8 e interferón g) que favorecen la expresión del factor tisular, trombomodulina y moléculas de adhesión endotelial que activan la fibrinólisis [7], [8]. Estudios histopatológicos en pacientes han demostrado daño alveolar difuso con infiltración de células T perivasculares, membranas celulares alteradas y características angiovasculares distintivas con presencia de trombosis y microangiopatía en los vasos pulmonares [9].…”

Section: Discussionunclassified

Tromboembolia pulmonar como complicación de COVID-19 en el puerperio. Reporte de un caso

Maldonado¹,

C²,

Contreras³

2020

Rev. chil. anest.

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El 31 de diciembre de 2019, se detectó en la ciudad de Wuhan (China) un brote de neumonía por un nuevo coronavirus designado como SARS-CoV-2. Desde el punto de vista clínico se encontró que los pacientes pueden desarrollar desde un cuadro leve de afección en vías respiratorias altas hasta cuadros de neumonía grave que se asocian a distrés respiratorio progresando a insuficiencia respiratoria grave. Se ha descrito que la infección predispone a fenómenos de hipercoagulabilidad y trombosis de localización venosa, reconociendo el tromboembolismo pulmonar (TEP) como el más frecuente. El embarazo es un estado fisiológico con alto riesgo para el desarrollo de complicaciones tromboembólicas, aumentando los factores de riesgo para TEP durante el parto y puerperio. En el contexto de la asociación de infección por SARS-CoV-2 y embarazo existen pocos informes alrededor del mundo al ser una patología reciente. En México, según registros epidemiológicos oficiales, el COVID-19 se ha convertido en la principal causa de muerte materna superando a los eventos preclámpticos y la hemorragia obstétrica, que hasta hace algunos meses, eran la primera causa. Se presenta el caso de una paciente diagnosticada con el nuevo coronavirus que, en el curso del puerperio mediato, desarrolla tromboembolia pulmonar causándole la muerte.

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“…Several markers of platelet and endothelial activation/injury, including soluble P-selectin, soluble thrombomodulin, and von Willebrand factor (vWf), were higher in critically ill COVID-19 patients than in noncritically ill patients and healthy controls, suggesting that platelets and endothelial cells are involved in the infection pathophysiology. The frequency of thrombotic events is approximately nine-fold higher in COVID-19 patients with dyslipidemia than in those without ( 101 , 102 ). A recent report linked dyslipidemia, hypertension, and endotheliopathy and demonstrated that lipids (enhanced by low-density lipoproteins), rapid blood flow, and a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) modulate the formation of secreted vWf into long fibrils tethered to endothelial cells ( 103 , 104 ).…”

Section: Covid-19 Disease Mechanisms In Organ Failurementioning

confidence: 94%

Severe Acute Respiratory Syndrome–Associated Coronavirus 2 Infection and Organ Dysfunction in the ICU: Opportunities for Translational Research

Verhoef

Kannan

Sturgill

et al. 2021

Critical Care Explorations

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Objectives: Since the beginning of the coronavirus disease 2019 pandemic, hundreds of thousands of patients have been treated in ICUs across the globe. The severe acute respiratory syndrome–associated coronavirus 2 virus enters cells via the angiotensin-converting enzyme 2 receptor and activates several distinct inflammatory pathways, resulting in hematologic abnormalities and dysfunction in respiratory, cardiac, gastrointestinal renal, endocrine, dermatologic, and neurologic systems. This review summarizes the current state of research in coronavirus disease 2019 pathophysiology within the context of potential organ-based disease mechanisms and opportunities for translational research. Data Sources: Investigators from the Research Section of the Society of Critical Care Medicine were selected based on expertise in specific organ systems and research focus. Data were obtained from searches conducted in Medline via the PubMed portal, Directory of Open Access Journals, Excerpta Medica database, Latin American and Caribbean Health Sciences Literature, and Web of Science from an initial search from December 2019 to October 15, 2020, with a revised search to February 3, 2021. The medRxiv, Research Square, and clinical trial registries preprint servers also were searched to limit publication bias. Study Selection: Content experts selected studies that included mechanism-based relevance to the severe acute respiratory syndrome–associated coronavirus 2 virus or coronavirus disease 2019 disease. Data Extraction: Not applicable. Data Synthesis: Not applicable. Conclusions: Efforts to improve the care of critically ill coronavirus disease 2019 patients should be centered on understanding how severe acute respiratory syndrome–associated coronavirus 2 infection affects organ function. This review articulates specific targets for further research.

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Tromboembolismo pulmonar y COVID-19: un cambio de paradigma

Cited by 7 publications

References 14 publications

Estimation of Admission D-dimer Cut-off Value to Predict Venous Thrombotic Events in Hospitalized COVID-19 Patients: Analysis of the SEMI-COVID-19 Registry

Estimation of Admission D-dimer Cut-off Value to Predict Venous Thrombotic Events in Hospitalized COVID-19 Patients: Analysis of the SEMI-COVID-19 Registry

Tromboembolia pulmonar como complicación de COVID-19 en el puerperio. Reporte de un caso

Severe Acute Respiratory Syndrome–Associated Coronavirus 2 Infection and Organ Dysfunction in the ICU: Opportunities for Translational Research

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