scholarly journals Characteristics and treatment of coagulopathy associated with COVID-19

2021 ◽  
Vol 72 (3) ◽  
pp. 70-77
Author(s):  
Predrag Miljić

Coagulopathy in COVID-19 represents a thrombo-inflammatory condition, and it is one of the most important causes of morbidity and mortality in this disease. The occurrence of coagulopathy correlates with the intensity of the inflammatory response to SARS-Cov-2 virus infection, and its presence is characterized by laboratory markers of blood hypercoagulability and clinically pronounced prothrombotic condition. Although the mechanism of coagulopathy is not fully elucidated, dysregulated and overemphasized immune responses mediated by inflammatory cytokines, complement activation, leukocyte activation with release of free nucleic acids and histones into the circulation, hypoxia and endothelial damage play a very important role in its development. Thrombosis can occur in all parts of the circulatory system and is most often localized in the microcirculation and venous part of the vasculature. A number of studies have shown that the presence of thrombotic pulmonary embolism can be demonstrated by objective methods in approximately 15% of COVID-19 patients treated in intensive care units, while the incidence of total venous thromboembolism in this group of patients is over 20% despite antithrombotic prophylaxis. Although much less common than venous thrombosis, arterial thrombosis may also occur in COVID-19 patients, most often in the form of myocardial infarction, ischemic stroke and peripheral artery occlusion. Damage to the endothelium under the influence of virus or inflammatory response, activation of platelets and coagulation system with fibrin deposition leads to extensive thrombosis in the microcirculation of lungs and other tissues and directly contributes to respiratory failure, ARDS or multiorgan failure. Therefore, coagulopathy in COVID-19 is an integral part of the pathophysiological mechanism of the disease and contributes to its clinical manifestation and progression. Main laboratory characteristics of COVID-19 coagulopathy are elevated values of D-dimer in the blood, which occurs in the process of decomposition of precipitated fibrin under the action of fibrinolytic enzymes in the microcirculation of the lungs and other organs. Therefore, D-dimer values reflect the intensity of the inflammation in the lungs and have prognostic significance in recognizing patients at risk of serious complications and unfavorable course of the disease. In contrast to disseminated intravascular coagulation in sepsis, severe thrombocytopenia and hypofibrinogenemia as well as bleeding tendencies are rare in COVID-19 coagulopathy. Due to the high frequency and important role of coagulopathy in morbidity and mortality, the use of anticoagulant therapy is recommended in all hospitalized patients. However, the optimal way of treating coagulopathy and the intensity of antithrombotic prophylaxis are not known, and represent the subject of intensive research.

2018 ◽  
Vol 10 (2) ◽  
pp. 90-95
Author(s):  
A. N. Kholodnaya ◽  
D. A. Lioznov ◽  
S. L. Nikolaenko ◽  
E. A. Blokhina ◽  
T. S. Yaroslavtseva ◽  
...  

Interleukin 6 and D-dimer known as chronic systemic inflammation markers shown prognostic significance in course of HIVdisease. Association between opioid use and systemic inflammation response are still elucidate. Objective: аssess plasma levels of IL-6 and D-dimer in HIV-positive patients in groups formed on the base of opiate use activity. Materials and methods. Crosssectional study of 346 HIV-positive ART-naive individuals. Participants were categorized into 3 groups according to their history of opioid use: 1) current opioid use — past 30 day opioid use; 2) «ever» opioid use — no use in past 30 days; 3) «never» opioid use. Results. Рarticipants with current opioid use had higher log-transformed IL-6 (0,4 [ s 1,0]; p<0,0001) and D-dimer (-0,6 [ s 0,9]; p<0,0001) levels than participants who reported «ever» (-0,1 [ s 1,0] and -0,9 [ s 0,8]), or «never» (-0,4 [ s 0,7] and 1,3 [ s 0,7]) opioid use. Conclusion. Оpioid use in HIV-positive participants is associated with higher inflammatory response.


Viruses ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 419
Author(s):  
Fares Qeadan ◽  
Benjamin Tingey ◽  
Lily Y. Gu ◽  
Ashley Hafen Packard ◽  
Esther Erdei ◽  
...  

Cytokine storm syndrome in patients with COVID-19 is mediated by pro-inflammatory cytokines resulting in acute lung injury and multiorgan failure. Elevation in serum ferritin and D-dimer is observed in COVID-19 patients. To determine prognostic values of optimal serum cutoff with trajectory plots for both serum ferritin and D-dimer in COVID-19 patients with invasive ventilator dependence and in-hospital mortality. We used retrospective longitudinal data from the Cerner COVID-19 de-identified cohort. COVID-19 infected patients with valid repeated values of serum ferritin and D-dimer during hospitalization were used in mixed-effects logistic-regression models. Among 52,411 patients, 28.5% (14,958) had valid serum ferritin and 28.6% (15,005) D-dimer laboratory results. Optimal cutoffs of ferritin (714 ng/mL) and D-dimer (2.1 mg/L) revealed AUCs ≥ 0.99 for in-hospital mortality. Optimal cutoffs for ferritin (502 ng/mL) and D-dimer (2.0 mg/L) revealed AUCs ≥ 0.99 for invasive ventilator dependence. Optimal cutoffs for in-house mortality, among females, were lower in serum ferritin (433 ng/mL) and D-dimer (1.9 mg/L) compared to males (740 ng/mL and 2.5 mg/L, respectively). Optimal cutoffs for invasive ventilator dependence, among females, were lower in ferritin (270 ng/mL) and D-dimer (1.3 mg/L) compared to males (860 ng/mL and 2.3 mg/L, respectively). Optimal prognostic cutoffs for serum ferritin and D-dimer require considering the entire trajectory of laboratory values during the disease course. Females have an overall lower optimal cutoff for both serum ferritin and D-dimer. The presented research allows health professionals to predict clinical outcomes and appropriate allocation of resources during the COVID-19 pandemic, especially early recognition of COVID-19 patients needing higher levels of care.


2021 ◽  
Vol 77 (18) ◽  
pp. 3031
Author(s):  
Diana Ronderos ◽  
Alaa Omar ◽  
Sayed Waqas Haider ◽  
Arsalan Rehmani ◽  
Alvaro Garcia Arenas ◽  
...  

Vestnik ◽  
2021 ◽  
pp. 103-106
Author(s):  
А.Е. Кожашева ◽  
С.О. Белесбек ◽  
Д.Ж. Абдимитова ◽  
Б.М. Сакен ◽  
А.П. Бориходжаева ◽  
...  

Появляются доказательства того, что COVID-19 может вызывать выброс цитокинов, состояние гиперкоагуляции и повреждение эндотелия, которое может привести к острому нарушению мозгового кровообращения (ОНМК). В данной статье авторы обсуждают взаимосвязь между COVID-19 и ОНМК, и о возможных факторах, способствующих возникновению инсульта. Как свидетельствует увеличение D-димера, фибриногена, фактора VIII и фактора фон Виллебранда, инфекция SARS-CoV-2 вызывает коагулопатию, нарушает функцию эндотелия и способствует состоянию гиперкоагуляции. В совокупности это предрасполагает пациентов к цереброваскулярным нарушениям. Механизм, лежащий в основе COVID-19 и инсульта, требует дальнейшего изучения, равно как и разработка эффективных терапевтических или профилактических мер. Evidence is emerging that COVID-19 can cause cytokine release, hypercoagulable states, and endothelial damage that can lead to acute cerebrovascular accident (ACVI). In this article, the authors discuss the relationship between COVID-19 and stroke and the possible contributing factors to stroke. As evidenced by an increase in D-dimer, fibrinogen, factor VIII and von Willebrand factor, SARS-CoV-2 infection causes coagulopathy, disrupts endothelial function and hypercoagulability. Collectively, this predisposes patients to cerebrovascular disorders. The mechanism underlying COVID-19 and stroke requires further study, as does the development of effective therapeutic or preventive measures.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Ivo A van der Bilt ◽  
Djo Hasan ◽  
W. P Vandertop ◽  
Arthur A Wilde ◽  
Ale Algra ◽  
...  

Cardiac complications after subarachnoid hemorrhage (SAH) occur frequently, but their prognostic significance remains unclear. We performed a meta-analysis to assess whether echocardiographic wall motion abnormalities (WMA), electrocardiographic (ECG) changes, or elevated markers for myocardial damage are related to the occurrence of delayed cerebral ischemia (DCI) or death. Methods All articles that reported on cardiac abnormalities after aneurysmal SAH, that met predefined criteria, and were published between 1960 and 2007 were assessed. Data were extracted on predefined methodological criteria, patient characteristics, prevalence of cardiac abnormalities, and DCI or death. We calculated pooled relative risks (RR) with corresponding 95% confidence intervals (CI) for the separate cardiac abnormalities and outcome. Results We included 25 studies (16 prospective), comprising 2690 patients (mean age 53 years; 35% was male). The figure shows the univariable RRs of the determinants for death. For DCI we found a significant association with WMA (RR 2.10 [CI 1.17, 3.78]); Troponin RR 3.15 [CI 2.27, 4.38]; CK-MB RR: 2.90 [CI 1.86, 4.52]; BNP RR: 4.52 [CI 1.79, 11.39]; and ST depression RR: 2.40 [CI 1.2, 4.9]. No significant associations were found for DCI and ST elevation RR: 2.1 [CI 0.7, 5.7]; T wave abnormality RR: 0.9 [CI 0.5, 1.7]; U wave RR: 0.7 [CI 0.4, 1.3] or prolonged QT RR: 1.0 [CI 0.5, 2.3]. Conclusion Cardiac abnormalities increase the risk of DCI and death after SAH. Future research should be directed towards elucidating the multivariable relationship between the cardiac prognosticators, the pathophysiological mechanism and potential treatment options.


2021 ◽  
Author(s):  
Yuqi Zhou ◽  
Masako Nishikawa ◽  
Hiroshi Kanno ◽  
Tinghui Xiao ◽  
Takuma Suzuki ◽  
...  

A characteristic clinical feature of COVID-19 is the frequent occurrence of thrombotic events. Furthermore, many cases of multiorgan failure are thrombotic in nature. Since the outbreak of COVID-19, D-dimer testing has been used extensively to evaluate COVID-19-associated thrombosis, but does not provide a complete view of the disease because it probes blood coagulation, but not platelet activity. Due to this limitation, D-dimer testing fails to account for thrombotic events which occur despite low D-dimer levels, such as sudden stroke in young patients and autopsy-identified widespread microthrombi in multiple organs. Here we report the landscape of circulating platelet aggregates in COVID-19 obtained by large-scale single-cell image-based profiling and temporal monitoring of the blood of COVID-19 patients (n = 110). Surprisingly, our analysis shows the anomalous presence of excessive platelet aggregates in nearly 90% of all COVID-19 patients, including those who were not clinically diagnosed with thrombosis and those with low D-dimer levels (less than 1 ug/mL). Additionally, results indicate a strong link between the concentration of platelet aggregates and the severity and mortality of COVID-19. Finally, high-dimensional analysis and comparison with other diseases reveal that COVID-19 behaves as a product of thrombosis (localized) and infectious diseases (systemic), as a cause of systemic thrombosis.


2004 ◽  
Vol 132 (5-6) ◽  
pp. 182-186 ◽  
Author(s):  
Dragan Milic ◽  
Miljko Pejic ◽  
Sasa Zivic ◽  
Aleksandar Karanikolic ◽  
Slobodan Jovanovic ◽  
...  

Systemic inflammatory response syndrome and sepsis are common in surgically treated patients. Systemic inflammatory response syndrome represents a major factor of morbidity and mortality in these patients. The pathogenesis of these syndromes has been increasingly clarified. The objective of this review is to present an overview of our current understanding of the physiology underlying these conditions. <br><br><font color="red"><b> This article has been retracted. Link to the retraction <u><a href=http://dx.doi.org/10.2298/SARH1206269U>10.2298/SARH1206269U</a><u></b></font>


Sign in / Sign up

Export Citation Format

Share Document