Disseminated intravascular coagulation: clinical and biological diagnosis

Risk factors for secondary hemophagocytic lymphohistiocytosis in severe coronavirus disease 2019 adult patients

“…Acute kidney injury (AKI) was diagnosed using the KDIGO criteria [11]. Prothrombin time test, the levels of fibrin/fibrinogen (Fib) degradation products, and platelet counts were used for the diagnosis of disseminated intravascular coagulation (DIC) [12]. Diagnosis of septic shock was based on the Third International Consensus Definition for Sepsis and Septic Shock [13].…”

Improved Detection of Anterior Circulation Occlusions: The “Delayed Vessel Sign” on Multiphase CT Angiography

“…30 In addition, the delayed vessel sign will be absent in cases of small cortical infarcts, which are often caused by occlusion of small pial vessels by microemboli. 31 The sign may falsely indicate an acute intracranial occlusion in several scenarios not encountered in this study population, for example in the setting of chronic intracranial occlusions/ stenoses and acute or chronic extracranial occlusions. Readers were not timed on their interpretation of the entire angiographic dataset but only on the time to establish the presence or absence of a vessel occlusion.…”

Coagulação intravascular disseminada: uma abordagem diagnóstica

“…The clinical and laboratory manifestations present in disseminated intravascular coagulation and its evolution and classification are determined by the underlying disease 8 . Acute disseminated intravascular coagulation can be manifested by hemorrhagic conditions, as gingival hemorrhage, petechiae, epistaxis, hematomas, and gastrointestinal bleeding 9 . Those manifestations are due to the exacerbated consumption of coagulation factors and platelets with the consequent decreased hemostatic capacity 8 .…”

“…Those manifestations are due to the exacerbated consumption of coagulation factors and platelets with the consequent decreased hemostatic capacity 8 . Moreover, due to excess generated thrombin, there is the susceptibility of the occurrence of thrombotic manifestations in the microvasculature and medium caliber vessels that can result from skin lesions, neurological disturbances, gangrene of the extremities, oliguria, and others, that is, malfunction of multiple organs, especially the lungs and kidneys 2,9 . Finally, the laboratory alterations found are: increased fibrin degradation products and do D-dimer, thrombocytopenia (< 50,000/μL) and prolonged prothrombin time (PT), and activated partial thromboplastin time (aPTT) 2 .…”

“…The clinical presentations are predominantly thrombotic, which can be: hyperthermia, hypotension, hemolytic anemia due to microangiopathy, and others. The laboratory alterations can be presented as slight thrombocytopenia and slightly prolonged or normal 2,9 .…”