Sepsis is a major cause of morbidity and mortality worldwide. Sepsis-associated coagulation disorders are involved in the pathogenesis of multiorgan failure and lead to a subsequently worsening prognosis. Alongside the global impact of the COVID-19 pandemic, a great number of research papers have focused on SARS-CoV-2 pathogenesis and treatment. Significant progress has been made in this regard and coagulation disturbances were once again found to underlie some of the most serious adverse outcomes of SARS-CoV-2 infection, such as acute lung injury and multiorgan dysfunction. In the attempt of untangling the mechanisms behind COVID-19-associated coagulopathy (CAC), a series of similarities with sepsis-induced coagulopathy (SIC) became apparent. Whether they are, in fact, the same disease has not been established yet. The clinical picture of CAC shows the unique feature of an initial phase of intravascular coagulation confined to the respiratory system. Only later on, patients can develop a clinically significant form of systemic coagulopathy, possibly with a consumptive pattern, but, unlike SIC, it is not a key feature. Deepening our understanding of CAC pathogenesis has to remain a major goal for the research community, in order to design and validate accurate definitions and classification criteria.

SARS-CoV-2 infection is a significant health concern that needs to be addressed not only during the initial phase of infection but also after hospitalization. This is the consequence of the various pathologies associated with long COVID-19, which are still being studied and researched. Lung fibrosis is an important complication after COVID-19, found in up to 71% of patients after discharge. Our research is based on scientific articles indexed in PubMed; in the selection process, we used the following keywords: “lung fibrosis”, “fibrosis mediators”, “fibrosis predictors”, “COVID-19”, “SARS-CoV-2 infection”, and “long COVID-19”. In this narrative review, we aimed to discuss the current understanding of the mechanisms of initiation and progression of post-COVID-19 lung fibrosis (PC-19-LF) and the risk factors for its occurrence. The pathogenesis of pulmonary fibrosis involves various mediators such as TGF-β, legumain, osteopontin, IL-4, IL-6, IL-13, IL-17, TNF-α, Gal-1, Gal-3, PDGF, and FGFR-1. The key cellular effectors involved in COVID-19 lung fibrosis are macrophages, epithelial alveolar cells, neutrophils, and fibroblasts. The main fibrosis pathways in SARS-CoV-2 infection include hypoxemia-induced fibrosis, macrophage-induced fibrosis, and viral-fibroblast interaction-induced fibrosis.

Background and Objectives: Pulmonary fibrosis represents a stage of normal physiologic response to inflammatory aggression, mostly self-limiting and reversible; however, numerous patients treated for SARS-CoV-2 pneumonia present after release from hospital residual lung fibrosis. In this article, we aim to present an optimization method for evaluating pulmonary fibrosis by quantitative analysis, to identify the risk factors/predictors for pulmonary fibrosis in patients with SARS-CoV-2 infection, and to characterize the impact of pulmonary fibrosis on the symptomatology of patients after release from the hospital. Materials and Methods: We performed a prospective observational study on 100 patients with severe forms of pneumonia, with a control group of 61 non-COVID normal patients. Results: We found persistent interstitial changes consistent with fibrotic changes in 69% of patients. The risk of fibrosis was proportional to the values of erythrocyte sedimentation rate (ESR), C reactive protein (CRP), and lactate dehydrogenase (LDH), and to the duration of hospitalization. The imaging parameters correlated with increased risk for interstitial fibrosis were the number of affected pulmonary lobes and the percent of interstitial pulmonary fibrosis. Conclusions: The main risk factors for pulmonary fibrosis post-COVID-19 identified in our study are increased ESR, CRP, LDH, duration of hospitalization and the severity of pneumonia.

Background and Objectives: SARS-CoV-2 has an extensive tissue tropism due to its ability to attach to the surfaces of cells through different receptors, leading to systemic complications. In this article, we aim to present the prevalence of pericardial effusions in patients with severe COVID-19, to identify the risk factors/predictors for pericardial involvement, and to evaluate its impact on overall mortality. Materials and Methods: We enrolled 100 patients with severe COVID-19 in our observational cohort study and divided them in two groups: Group A (27 patients with pericardial effusion) and Group B (73 patients without pericardial effusion). We recorded demographic and lifestyle parameters, anthropometric parameters, clinical parameters, inflammation markers, respiratory function parameters, complete blood count, coagulation parameters, and biochemical serum parameters. All patients were evaluated by computer tomography scans within 48 h of admission. Results: The median age was 61 years in both groups and the male/female ratio was 3.5 vs. 2.8 in Group A vs. Group B. We identified mild pericardial effusion (3–4 mm) in 62.9% patients and moderate pericardial effusion (5–9 mm) in 37.1% patients, with a median value of 4 [3;6] mm. The patients with pericardial effusion presented with higher percentages of obesity, type-2 diabetes mellitus, arterial hypertension, and congestive heart failure, without statistical significance. Increased values in cardiac enzymes (myoglobin, CK, CK-MB) and LDH were statistically associated with pericardial effusion. The overall mortality among the participants of the study was 24% (24 patients), 33.3% in Group A and 20.8% in Group B. Conclusions: Pericardial effusion has a high prevalence (27%) among patients with severe forms of COVID-19 and was associated with higher mortality. Pericardial effusion in our study was not associated with the presence of comorbidities or the extent of lung involvement. Overall mortality was 60% higher in patients with pericardial effusion.

Background and Objectives: The severe forms of SARS-CoV-2 pneumonia are associated with acute hypoxic respiratory failure and high mortality rates, raising significant challenges for the medical community. The objective of this paper is to present the importance of early quantitative evaluation of radiological changes in SARS-CoV-2 pneumonia, including an alternative way to evaluate lung involvement using normal density clusters. Based on these elements we have developed a more accurate new predictive score which includes quantitative radiological parameters. The current evolution models used in the evaluation of severe cases of COVID-19 only include qualitative or semi-quantitative evaluations of pulmonary lesions which lead to a less accurate prognosis and assessment of pulmonary involvement. Materials and Methods: We performed a retrospective observational cohort study that included 100 adult patients admitted with confirmed severe COVID-19. The patients were divided into two groups: group A (76 survivors) and group B (24 non-survivors). All patients were evaluated by CT scan upon admission in to the hospital. Results: We found a low percentage of normal lung densities, PaO₂/FiO₂ ratio, lymphocytes, platelets, hemoglobin and serum albumin associated with higher mortality; a high percentage of interstitial lesions, oxygen flow, FiO₂, Neutrophils/lymphocytes ratio, lactate dehydrogenase, creatine kinase MB, myoglobin, and serum creatinine were also associated with higher mortality. The most accurate regression model included the predictors of age, lymphocytes, PaO₂/FiO₂ ratio, percent of lung involvement, lactate dehydrogenase, serum albumin, D-dimers, oxygen flow, and myoglobin. Based on these parameters we developed a new score (COV-Score). Conclusions: Quantitative assessment of lung lesions improves the prediction algorithms compared to the semi-quantitative parameters. The cluster evaluation algorithm increases the non-survivor and overall prediction accuracy.COV-Score represents a viable alternative to current prediction scores, demonstrating improved sensitivity and specificity in predicting mortality at the time of admission.

Background and Objectives: The microanatomy of the superior cerebellar artery (SCA) is clinically significant. We, thus, aimed at patterning unilateral and bilateral possibilities of SCA origin. Materials and Methods: In total, 205 archived records of computed tomography and magnetic resonance angiograms were used. There were defined types of SCA origin from the basilar artery (BA): “0”—absent SCA, “1”—preterminal, “2”—collateral SCA, with SCA appearing as a terminal branch of BA, and “3”—SCA from the posterior cerebral artery (PCA) of the cerebral type. Fenestrations and duplications of SCA were recorded. Bilateral combinations of types were recorded as follows: A (1 + 0), B (1 + 1), C (1 + 2), D (1 + 3), E (1 + duplicated SCA), F (2 + 2), G (2 + 3), H (3 + 3), I (3 + duplicated SCA), J (1 + fenestrated SCA). Results: Type 0 SCAs were found in 0.25%, type 1 in 71.29%, type 2 in 19.06%, and type 3 in 9.41%. Absent and fenestrated SCAs were each found in a single case. The most frequent combinations were B (58.05%), C (13.17%) and F (13.17%). Bilateral symmetrical types occurred in 70.7% of cases. Fetal types of PCA and the artery of Percheron modified the BA ends. Combinations of C, F, and G changed the BA ends or tips; thus, different subtypes resulted in five BA bifurcation patterns, including five BA trifurcations and one BA quadrifurcation. BA trifurcation was also found in cases with duplicated SCAs. Conclusions: The SCA has various anatomical possibilities of origin and bilateral combinations that are not presented in anatomical lectures. Details on the specific end of the BA should be gathered on a case-by-case basis.