Abstract:The autopsy findings for 3 cases of SARS-(CoV-2) pneumonia-related deaths are reported with pulmonary histology and immunohistochemistry findings. In 2 cases (cases 1 and 2), the time interval from presentation to death was approximately 1 week, whereas for case 3, the time interval from presentation to death was hours. Case 1 and case 2 presented with shortness of breath, cough, and flu-like symptoms. The decedent from case 3 died shortly after presenting to a local emergency room with high fever, chest and a… Show more
“…Pulmonary artery (PA) thrombosis is a potential complication in severe COVID-19 despite the administration of anticoagulation treatment [5]. In accordance with the theory that endothelium damage is caused by SARS-CoV-2 are several post-mortem autopsy studies, in which diffuse alveolar damage and atypical cells that are thought to be endothelial cells infected via the human angiotensin-converting enzyme 2 receptor (hACE2R) are common findings [6][7][8][9].…”
Coronavirus disease 2019 (COVID-19) pneumonia is associated with extensive pulmonary microangiopathy and the enlargement of the pulmonary artery (PA), while its progression after the remission of the disease has not been investigated yet. The aim was to assess the diametral increase in the PA in COVID-19 pneumonia, as revealed on chest computed tomography (CT), and further investigate its progression. This was a retrospective cohort study of patients with COVID-19 pneumonia, without prior history of pulmonary hypertension, who underwent CT pulmonary angiography before, during, and after the infection. Pulmonary embolism was excluded in all cases. The main PA diameter (MPAD) was assessed in consecutive chest imaging. Statistical analysis was performed with the non-parametric Wilcoxon and Kruskal–Wallis tests, while correlations were performed with the non-parametric Spearman test. A mean ± SD MPAD of 3.1 ± 0.3 cm in COVID-19 pneumonia was significantly decreased to 2.8 ± 0.3 cm in the post-infectious state after 2–18 months in 31 patients (p-value: <0.0001). In a subgroup of six patients with more than one post-COVID-19 CT, a significant further decline in the diameter was observed (p-value: 0.0313). On the other hand, in accordance with the literature, a significant increase in the MPAD during COVID-19 pneumonia was noted in a group of 10 patients with a pre-COVID-19 CT (p-value: 0.0371). The enlargement of the PA is a common finding in COVID-19 pneumonia that regresses after the remission of the disease, indicating that this reversible cardiovascular event is a potential marker of disease activity, while its course in long COVID is yet to be determined.
“…Pulmonary artery (PA) thrombosis is a potential complication in severe COVID-19 despite the administration of anticoagulation treatment [5]. In accordance with the theory that endothelium damage is caused by SARS-CoV-2 are several post-mortem autopsy studies, in which diffuse alveolar damage and atypical cells that are thought to be endothelial cells infected via the human angiotensin-converting enzyme 2 receptor (hACE2R) are common findings [6][7][8][9].…”
Coronavirus disease 2019 (COVID-19) pneumonia is associated with extensive pulmonary microangiopathy and the enlargement of the pulmonary artery (PA), while its progression after the remission of the disease has not been investigated yet. The aim was to assess the diametral increase in the PA in COVID-19 pneumonia, as revealed on chest computed tomography (CT), and further investigate its progression. This was a retrospective cohort study of patients with COVID-19 pneumonia, without prior history of pulmonary hypertension, who underwent CT pulmonary angiography before, during, and after the infection. Pulmonary embolism was excluded in all cases. The main PA diameter (MPAD) was assessed in consecutive chest imaging. Statistical analysis was performed with the non-parametric Wilcoxon and Kruskal–Wallis tests, while correlations were performed with the non-parametric Spearman test. A mean ± SD MPAD of 3.1 ± 0.3 cm in COVID-19 pneumonia was significantly decreased to 2.8 ± 0.3 cm in the post-infectious state after 2–18 months in 31 patients (p-value: <0.0001). In a subgroup of six patients with more than one post-COVID-19 CT, a significant further decline in the diameter was observed (p-value: 0.0313). On the other hand, in accordance with the literature, a significant increase in the MPAD during COVID-19 pneumonia was noted in a group of 10 patients with a pre-COVID-19 CT (p-value: 0.0371). The enlargement of the PA is a common finding in COVID-19 pneumonia that regresses after the remission of the disease, indicating that this reversible cardiovascular event is a potential marker of disease activity, while its course in long COVID is yet to be determined.
“…Although the majority of infections are asymptomatic to mild, acute respiratory distress syndrome has widely been reported, especially in patients with multiple comorbidities. Vascular abnormalities have also been reported in the literature and include endotheliitis, thromboemboli, and atypical endovascular cell morphology 1,2 …”
mentioning
confidence: 96%
“…Vascular abnormalities have also been reported in the literature and include endotheliitis, thromboemboli, and atypical endovascular cell morphology. 1 , 2 …”
mentioning
confidence: 99%
“…Vascular abnormalities have also been reported in the literature and include endotheliitis, thromboemboli, and atypical endovascular cell morphology. 1,2 Isolated arterial dissection occurring without aortic dissection is uncommon but has been reported in the carotid arteries and renal arteries. The splanchnic circulation comprises the gastric, pancreatic, hepatic, splenic, and intestinal circulations.…”
Spontaneous multiple arterial dissection (SMAD) is a rarely reported phenomenon and has been previously linked to connective tissue diseases and specifically the genetic mutations in
SMAD3
and
COL3A1
. Herein we describe a case of SMAD with scattered thrombi in a COVID-19–positive patient with a history of unspecified mitochondrial myopathy. Vasculopathy involved the splenic artery, inferior mesenteric artery, internal mammary arteries, omental arteries, mesenteric arteries, and small renal arteries. Dissections were confirmed by histology in the splenic artery, inferior mesenteric artery, and bilateral renal medullary arteries. Genetic studies were done to rule out
SMAD3
and
COL3A1
mutations. Because the Smad3 protein has been previously implicated in COVID-19–associated tissue fibrosis, it may play a role in endothelial dysfunction as well.
Background
Limited clinical data suggest ~16% prevalence of bacterial superinfections among critically ill patients with coronavirus disease 2019 (COVID-19).
Methods
We reviewed postmortem studies of patients with COVID-19 published in English through 26 September 2020 for histopathologic findings consistent with bacterial lung infections.
Results
Worldwide, 621 patients from 75 studies were included. The quality of data was uneven, likely because identifying superinfections was not a major objective in 96% (72/75) of studies. Histopathology consistent with potential lung superinfection was reported in 32% (200/621) of patients (22-96 years old; 66% men). Types of infections were pneumonia (95%), abscesses or empyema (3.5%), and septic emboli (1.5%). Seventy-three percent of pneumonias were focal rather than diffuse. Predominant histopathologic findings were intra-alveolar neutrophilic infiltrations that were distinct from those typical of COVID-19-associated diffuse alveolar damage. In studies with available data, 79% of patients received antimicrobial treatment; most common agents were beta-lactam/beta-lactamase inhibitors (48%), macrolides (16%), cephalosoprins (12%), and carbapenems (6%). Superinfections were proven by direct visualization or recovery of bacteria in 25.5% (51/200) of potential cases, and 8% of all patients in postmortem studies. In rank order, pathogens included Acinetobacter baumannii, Staphylococcus aureus, Pseudomonas aeruginosa and Klebsiella pneumoniae. Lung superinfections were causes of death in 16% of potential cases, and 3% of all patients with COVID-19.
Conclusions
Potential bacterial lung superinfections were evident at postmortem examination in 32% of persons who died with COVID-19 (proven, 8%; possible, 24%), but they were uncommonly the cause of death.
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