fibrin and Coronavirus-Infections

In late December 2019 an outbreak of a novel coronavirus (SARS-CoV-2) causing severe pneumonia (COVID-19) was reported in Wuhan, Hubei Province, China. A common finding in most COVID-19 patients is high D-dimer levels which are associated with a worse prognosis. We aimed to evaluate coagulation abnormalities via traditional tests and whole blood thromboelastometry profiles in a group of 22 (mean age 67 ± 8 years, M:F 20:2) consecutive patients admitted to the Intensive Care Unit of Padova University Hospital for acute respiratory failure due to COVID-19. Cases showed significantly higher fibrinogen and D-dimer plasma levels versus healthy controls (

Topics: Acute Disease; Aged; Area Under Curve; Betacoronavirus; Blood Coagulation; Blood Coagulation Tests; Coronavirus Infections; COVID-19; Critical Care; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Humans; Intensive Care Units; Italy; Male; Middle Aged; Pandemics; Pneumonia, Viral; Prognosis; Respiration Disorders; SARS-CoV-2; Thrombelastography; Thrombophilia; Treatment Outcome

Forensic investigations generally contain extensive morphological examinations to accurately diagnose the cause of death. Thus, the appearance of a new disease often creates emerging challenges in morphological examinations due to the lack of available data from autopsy- or biopsy-based research. Since late December 2019, an outbreak of a novel seventh coronavirus disease has been reported in China caused by "severe acute respiratory syndrome coronavirus 2" (SARS-CoV-2). On March 11, 2020, the new clinical condition COVID-19 (Corona-Virus-Disease-19) was declared a pandemic by the World Health Organization (WHO). Patients with COVID-19 mainly have a mild disease course, but severe disease onset might result in death due to proceeded lung injury with massive alveolar damage and progressive respiratory failure. However, the detailed mechanisms that cause organ injury still remain unclear. We investigated the morphological findings of a COVID-19 patient who died during self-isolation. Pathologic examination revealed massive bilateral alveolar damage, indicating early-phase "acute respiratory distress syndrome" (ARDS). This case emphasizes the possibility of a rapid severe disease onset in previously mild clinical condition and highlights the necessity of a complete autopsy to gain a better understanding of the pathophysiological changes in SARS-CoV-2 infections.

Topics: Alveolar Epithelial Cells; Autopsy; Betacoronavirus; Coronavirus Infections; Cough; COVID-19; Diabetes Mellitus, Type 2; Fever; Fibrin; Fibrosis; Humans; Hyperplasia; Hypertension; Lung; Lymphocytes; Macrophages; Male; Megakaryocytes; Metaplasia; Middle Aged; Neutrophils; Pandemics; Pneumonia, Viral; Quarantine; SARS-CoV-2; Tachycardia; Thrombosis

A 75-year-old man presented to a French hospital with a 4-day fever after returning from a coronavirus disease-19 (COVID-19) cluster region. A reverse-transcription polymerase chain reaction test was positive for severe acute respiratory syndrome coronavirus-2 (SARS CoV-2) using a nasopharyngeal swab sample. After he returned home and a telephone follow-up, he was found deceased 9 days after first showing symptoms. Whole-body, non-enhanced, post-mortem computed tomography (PMCT) and a forensic autopsy were performed approximately 48 h after death, with sanitary precautions. The PMCT showed bilateral and diffuse crazy-paving lung opacities, with bilateral pleural effusions. Post-mortem virology studies detected the presence of SARS-CoV-2 (B.1 lineage) in the nasopharynx, plasma, lung biopsies, pleural effusion and faeces confirming the persistence of viral ribonucleic acid 48 h after death. Microscopic examination showed that severe lung damage was responsible for his death. The main abnormality was diffuse alveolar damage, associated with different stages of inflammation and fibrosis. This case is one of the first to describe complete post-mortem data for a COVID-19 death and highlights the ability of PMCT to detect severe involvement of the lungs before autopsy in an apparently natural death. The present pathology results are concordant with previously reported findings and reinforce the disease pathogenesis hypothesis of combined viral replication with an inappropriate immune response.

Topics: Aged; Alveolar Epithelial Cells; Autopsy; Betacoronavirus; Coronavirus Infections; COVID-19; Fibrin; Humans; Hyperplasia; Lung; Male; Pandemics; Pleural Effusion; Pneumonia, Viral; Pulmonary Alveoli; SARS-CoV-2; Tomography, X-Ray Computed