COVID-19: what the clinician should know about post-mortem findings
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EDITORIAL
COVID‑19: what the clinician should know about post‑mortem findings Danny Jonigk1,2, Bruno Märkl3 and Julie Helms4,5* © 2020 Springer-Verlag GmbH Germany, part of Springer Nature
As of September 2020, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has led to over 33 million infections and 1.000.000 deaths worldwide [1]. Compared to other coronavirus outbreaks (SARS-CoV-1, MERS-CoV), SARS-CoV-2 is characterized by a higher basic reproductive rate and an overall lower mortality [2]. However, while coronavirus disease 2019 (COVID-19) typically begins as an infection of the upper aerodigestive tract, it may progress to severe forms, with an acute respiratory distress syndrome (ARDS) and a multisystemic disease. COVID-19 ARDS shares the common histological hallmarks with other infectious/non-infectious ARDS. Unspecific diffuse alveolar damage (DAD), as its histologic correlate, is characterized by edema, hemorrhage and intra-alveolar fibrin deposition, but in case of COVID-19 ARDS, also by a distinct angiocentric lymphocytic inflammation [3–5]. DAD is the leading pattern of lung injury and has been shown to be independent of mechanical ventilation. There is some evidence for alternative injury patterns in COVID-19 ARDS, such as acute fibrinous organizing pneumonia (AFOP). Nonetheless, COVID-19-induced DAD is by far the most frequently reported one and is also characterized by more distinct morphologic features, including vascular changes [5]. In that, the detection of SARS-CoV-2 in multiple organs (respiratory tract, heart, endothelium, digestive tract, kidneys, brain) and multisystemic clinical features, suggest that COVID-19 might be a systemic “vascular disease” (Fig. 1). The vasculature indeed appears to be
*Correspondence: Julie.helms@chru‑strasbourg.fr 4 Service de Médecine Intensive‑Réanimation, Hôpitaux Universitaires de Strasbourg, Nouvel Hôpital Civil, 1, place de l’Hôpital, 67091 Strasbourg cedex, France Full author information is available at the end of the article
more than a mere means of virus propagation. After virus respiratory tract invasion, the cytokine storm secondary to the innate and adaptive immune responses, along with a potential direct cytopathic effect of the virus, are likely to trigger an endothelial dysfunction [6, 7]. SARS-CoV-2 thus leads to three distinctive angiocentric features with: i. endothelial damage associated with intracellular SARSCoV-2 virus, platelet activation, elevated D-dimers and fibrinogen; ii. widespread vascular thrombosis, and iii. abnormal vascular architecture (intussusceptive neoangiogenesis), suggesting microangiopathy [8] and resulting in disrupted laminar blood flow and vasoconstriction. This special form of vascularization is thought to act as an aberrant reaction to the viral aggression [4, 9]. The extensive endothelial damage seen in postmortem examinations also suggested viral inclusions being critically involved, but also endothelial inflammation with mononuclear cell infiltrate and lymphocytic endotheliitis, whic
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