1985
DOI: 10.1097/00000433-198503000-00006
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Fluidity of cadaveric blood after sudden death: Part II

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Cited by 30 publications
(15 citation statements)
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“…Platelets and serum proteins retain their normal function a few hours after blood cessation; afterwards stasis, hypoxia, decreased pH, and endothelial alterations lead to the formation of postmortem blood cloths concomitant with fibrinolysis processes (19,20). In deaths in which increased levels of catecholamine or plasminogen activator are released in the agonal period (as is the case with most sudden deaths) the thrombolytic events are increased and the cadaveric blood is liquid; if the agonal period is prolonged thrombotic events are dominant, leading to an increased density of postmortem clots (21)(22)(23). For this reason we could not perform coagulation tests, that might have revealed the presence of additional risk factors for thromboembolism.…”
Section: Casementioning
confidence: 99%
“…Platelets and serum proteins retain their normal function a few hours after blood cessation; afterwards stasis, hypoxia, decreased pH, and endothelial alterations lead to the formation of postmortem blood cloths concomitant with fibrinolysis processes (19,20). In deaths in which increased levels of catecholamine or plasminogen activator are released in the agonal period (as is the case with most sudden deaths) the thrombolytic events are increased and the cadaveric blood is liquid; if the agonal period is prolonged thrombotic events are dominant, leading to an increased density of postmortem clots (21)(22)(23). For this reason we could not perform coagulation tests, that might have revealed the presence of additional risk factors for thromboembolism.…”
Section: Casementioning
confidence: 99%
“…Advanced atherosclerotic coronary disease is often co-existent, although little or no coronary atherosclerosis was detected in approximately half of the sudden cardiac death cases. In some cases, extremely acute ischemic changes of the myocardium were observed only with microscopically attentive examination, suggesting the possibility of antemortem spasm of coronary stem and disappearance of the coronary thrombus due to the enhanced postmortem fibrinolytic activity [2][3][4]. Some components in the blood seem to induce the coronary spasm and/or thrombogenesis under certain conditions, which does not necessarily relate with the severity of atherosclerosis.…”
Section: Introductionmentioning
confidence: 99%
“…In our opinion, the latter explanation is the most plausible, because high levels of catecholamines and low pH, as often seen in these (TE 96 ms, TR 4,000 ms). Note the hyperdensities in the lower areas of the right upper pulmonary lobe (small arrow) in contrast to the hypodensities of the upper parts (large arrow) and to the right lower lobe below; on coronal T2-weighted MR images, internal livores appear hypointense in contrast to other parenchymal organs (upper arrow) cases, induce fibrinolysis by increasing the release of plasminogen activator from the vascular wall [27][28][29]. Supporting this explanation is the experience that clotting mostly begins within the cardiac cavities and the major vessels.…”
Section: Postmortem Clottingmentioning
confidence: 99%