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Histopathology of the Lung in Asphyxiation, Suffocation and Pressure to the Neck
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Wolfgang Grellner, Burkhard Madea
As a central organ in the pathophysiology of asphyxiation, the lung may exhibit alterations of its microstructure and/or cell content. In this context the working group of Brinkmann et al. [3,4] established the diagnosis of asphyxiation by microscopic investigation of the lung: they emphasized characteristic pulmonary alterations such as emphysema, alveolar−septal oedema, hyperaemia and microhaemorrhages, which they named ‘haemorrhagic−dysoric syndrome’ due to enhanced permeability of membranes. In combination with microembolism syndrome, they regarded it as a tool to differentiate death by obstructive asphyxia from other causes of death with similarly short periods of agony. Janssen, in addition, observed the appearance of numerous alveolar macrophages and intra-alveolar giant cells in cases of protracted oxygen deficiency (throttling, smothering, thoracic compression), an agonal mobilization and proliferation of alveolar cells with the formation of multinuclear giant cells [9,10]. In contrast, Betz et al. [1,2] demonstrated that these cell populations appeared in both fatal asphyxia/suffocation (strangulation, drowning, thoracic compression, hypoxia) and control cases with very short survival periods with nearly the same frequency.
Coronary Artery Disease: Role of Antithrombotic Therapy *
Published in Hau C. Kwaan, Meyer M. Samama, Clinical Thrombosis, 2019
Valentin Fuster, Douglas H. Israel, Lina Badimon, James H. Chesebro
Recent evidence from our laboratory has shown that thrombosis occurring in the setting of plaque disruption is a dynamic process of coagulation combined with platelet aggregation and disaggregation. The equilibrium is shifted one way or the other by the relative balance between pro- and antithrombotic tendencies (i.e., the depth of injury). Disaggregating platelets may break free, resulting in downstream microemboli suggested by some to have a role in ischemic sudden death. Even when such microembolism occurs, rethrombosis is common due to persistence of a thrombogenic substrate and abnormal hemorheology.13 It appears likely that in the acute coronary syndromes multiple cycles of thrombotic occlusion and spontaneous thrombolysis may occur, with vasoconstriction also acting to promote arterial occlusion.14 Thus, plaque rupture with thrombosis results in a clinical spectrum which may manifest as worsening angina pectoris, unstable angina, myocardial infarction, or ischemic sudden death, depending, as we have suggested, upon the degree of obstruction caused by the thrombus, the duration of obstruction, and the suddenness of the obstruction.15
Procoagulant Activity and Lung Disease
Published in Gary A. Levy, Edward H. Cole, Procoagulant Activity in Health and Disease, 2019
Harold A. Chapman, John S. Munger, David A. Waltz
As illustrated in Figure 4, several aspects of the clinical presentation of ARDS can be at least partially explained by changes in the cellular expression of procoagulant and fibrinolytic pathways in the vascular and extravascular compartments. On the vascular surfaces, fibrin deposition both in the form of microembolism as a consequence of disseminated intravascular coagulation (DIC) and of in situ thromboses as a consequence of the endothelial cell injury has been documented.47,48 Microvascular angiography shows vascular occlusion in approximately half of all patients with ARDS, frequently at multiple sites, and this is confirmed by autopsy studies.49–51 Pulmonary vascular fibrin deposition in ARDS is likely clinically relevant. Obliteration of the vascular bed, accompanied by a rising pulmonary vascular resistance, is a well-documented and strong correlate with poor outcome in patients with ARDS.52 Moreover, fibrin degradation products are chemoattractive for leukocytes and fibroblasts, potentially contributing to the inflammatory process, and fibrin serves as a nidus for organization of a healing response leading potentially to permanent obliteration of capillaries.53–56
Determination of the LD50 with the chick embryo chorioallantoic membrane (CAM) assay as a promising alternative in nanotoxicological evaluation
Published in Nanotoxicology, 2021
Christoph Raphael Buhr, Jonas Eckrich, Martin Kluenker, Kai Bruns, Nadine Wiesmann, Wolfgang Tremel, Jürgen Brieger
In our experience administration of lower doses of ZnO NPs resulted in a lower survival compared to Zn2+ (ZnCl2). Clotting of capillary vessels by particles and associated microembolism, resulting in changes of the intravascular bloodstream may be attributable to this observation. After injecting ZnCl2 in high concentrations, petechial bleedings in the proximal femoral region of the embryo were observed. Although not the main investigational focus a possible connection between zinc concentrations and blood coagulation seems thinkable. As ADAMTS13 is a zinc-dependent enzyme that is important for platelet aggregation (Renz 2018) high concentrations of Zn2+ may inhibit this enzyme (Anderson, Kokame, and Sadler 2006; Han et al. 2011). This might account for the observed petechial bleedings after ZnCl2 injection. No bleedings were observed after injection of nanoparticulate ZnO, even when higher concentrations were applied.
Intra-arterial administration of cell-based biological agents for ischemic stroke therapy
Published in Expert Opinion on Biological Therapy, 2019
Stavros Spiliopoulos, Georgios Festas, Lazaros Reppas, Elias Brountzos
Cell-based therapies for ischemic stroke are invasive therapeutic procedures and as such could produce undesirable side effects. Until today, reported complications are directly related to the route of administration. First of all, intracerebral administration has been associated with headache, somnolence and subdural hematomas, as during stereotactically guided neurosurgical cell delivery there is a risk of inducing focal hemorrhage. Moreover, during intravascular administration vascular obstruction could occur, mainly cerebral microembolism during IA and pulmonary microembolism during IV administration. It should be highlighted that any selected route of administration, especially with allogenic or xenogenic sources, could activate immunological responses such as graft rejection and graft versus host disease (GvHD). In particular, graft rejection is induced by circulating antibodies and T cells which recognize foreign MHC molecules. As for GvHD, it is probably triggered when transplanted MHC misleads cells with leukocyte function [75,89].
Cardiac rehabilitation and its effects on cognition in patients with coronary artery disease and heart failure
Published in Expert Review of Cardiovascular Therapy, 2018
Kannayiram Alagiakrishnan, Darren Mah, Gabor Gyenes
Surgical management of CAD with coronary artery bypass grafting (CABG) has also been linked to CI [26]. Cardiac surgery may increase the risk of dementia by microembolism, intraoperative hypotension, hypoxia and/or by triggering a systemic inflammatory response. Surgery also causes tissue injury and release of inflammatory molecules which can cause neuronal dysfunction and lead to post-operative cognitive dysfunction [27,28]. Central nervous system immune cells play an integral role in propagating inflammatory signals that are believed to play a role in causing CI [29]. Rates of cognitive decline as high as 41% have been reported following CABG [30] and have been observed up to 5 years after surgery. However, a similar degree of cognitive decline was also reported in patients with CAD who did not undergo bypass surgery [30]. A meta-analysis of randomized controlled trials of patients undergoing CABG showed similar results and also found that cardiopulmonary bypass in and of itself did not have a significant effect on cognition [31].