Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 428
Filter
1.
Archives of Medical Research ; 2022.
Article in English | ScienceDirect | ID: covidwho-1821136

ABSTRACT

Aim of the study Development of thrombocytopenia and thrombosis after administration of the ChAdox1 nCoV-19 (AstraZeneca-Oxford) vaccine has recently been described. This new condition is called vaccine-induced immune thrombotic thrombocytopenia (VITT). Our objective was to summarize case reports on VITT with/without D-dimer increments in AstraZeneca-Oxford vaccinated individuals. Data sources MEDLINE, PubMed, and Scopus databases were searched. Study selection Case series, case reports, letters to the editor;and s of AstraZeneca-Oxford vaccinated patients with a clinical profile of thrombocytopenia (platelet count <150X10 3 /dL) and D-dimer determination, with or without thrombosis, and/or bleeding, and/or antibodies against platelet factor 4 (aPF4), were included. Data extraction Baseline risk factors, symptoms, physical signs;laboratory results, imaging findings, treatment;and outcome in patients with VITT reported in case series, were examined. Data synthesis Patients who developed VITT were more likely to be young women (ages 21 to 77) given the AstraZeneca-Oxford vaccine 5–14 days prior to presentation. Patients’ signs, symptoms, and imaging findings were consistent with cerebral venous sinus thrombosis, or deep veins, lung, and other sites. Laboratory findings showed thrombocytopenia, low fibrinogen, and elevated D-dimer levels, while aPF4 was positive in most assays performed. Treatment was non-heparin anticoagulants, IV immunoglobulin, and steroids, as recommended by medical guidelines. Conclusions Vaccine-induced immune thrombotic thrombocytopenia is a rare complication with high morbidity, related to administration of the AstraZeneca-Oxford vaccine. Clinicians should prepare for early identification of patients with suspicious symptoms, and prompt treatment initiated to avoid catastrophic events. D-dimer determination is useful for surveillance of cases with suspected VITT.

2.
Ejves Vascular Forum ; 54:41-43, 2022.
Article in English | Web of Science | ID: covidwho-1814381

ABSTRACT

Introduction: Acute thrombosis of an infrarenal abdominal aortic aneurysm (ATAAA) represents an uncommon but catastrophic pathology, which can lead to life threatening complications. This is a report of the infrequent use of an endovascular solution to successfully treat ATAAA in a patient with COVID-19 viral pneumonia and ischaemia induced lower extremity neurological deficits. Report: An 89 year old white male, with a history of cardiovascular comorbidities was admitted to the emergency room with dyspnoea associated with the sudden onset of abdominal and back pain followed by partial motor and sensory deficits in both legs. The CT scan showed both an 8 cm infrarenal AAA with middle (inferior mesenteric artery patent) and distal thrombotic occlusion of the sac and non-aneurysmal but thrombosed common iliac arteries. An additional finding was imaging features typical of interstitial pneumonia. After the molecular test detected active COVID-19 infection, the patient was treated as an emergency with an aorto-uni-iliac stent graft and femorofemoral crossover graft. The post-operative course was uneventful with AAA exclusion and disappearance of ischaemic symptoms. There were no vascular complications. At three month follow up the patient remained asymptomatic and was looking after himself. Discussion: This case supports the feasibility and safety of a minimally invasive endovascular procedure to treat ATAAA in selected patients with favourable anatomy and high risk of respiratory complications in the context of the COVID-19 pandemic. (C) 2022 The Author(s). Published by Elsevier Ltd on behalf of European Society for Vascular Surgery.

3.
J Med Cases ; 13(4):168-171, 2022.
Article in English | PubMed | ID: covidwho-1811544

ABSTRACT

Coronavirus disease 2019 (COVID-19) causes various hematological abnormalities, leading to several complications in the disease course. We report two COVID-19 cases presenting with a combination of thrombocytopenia and coagulopathy complications in late 2020. A 73-year-old male with a history of immune thrombocytopenic purpura (ITP) presented with acute ischemic stroke and acute thrombocytopenia in the setting of COVID-19. He was managed with steroids and intravenous immunoglobulin (IVIG) and had a subsequent acute ischemic stroke with microhemorrhages. Another 72-year-old female with a history of cryptogenic liver cirrhosis and chronic thrombocytopenia presenting with acute thrombocytopenia in the setting of COVID-19 was managed with steroids and IVIG. She had a coagulopathic complication of deep venous thrombosis (DVT) later in her disease course managed with inferior vena cava filter and low-dose enoxaparin, but she subsequently died with a bleeding complication of retroperitoneal hemorrhage. Despite the aggressive ongoing research, the treatment options for severe COVID-19 are limited to date and the mortality remains high. Both these cases are examples of challenging situations that the physicians are currently facing with COVID-19 pandemic.

4.
Respiratory Case Reports ; 11(1):19-24, 2022.
Article in English | EMBASE | ID: covidwho-1798778

ABSTRACT

COVID-19 coagulopathy has gained attention due to the strikingly high prevalence of deep vein thrombosis (DVT) and pulmonary embolism (PE). We describe here a case of bilateral PE preceded by mild COVID-19 contracted 4.5 months earlier in a male patient who presented to the outpatient clinic with exertional dyspnea. The patient had developed PE 9 years earlier, when no underlying genetic factor was detected. In the 4.5 months after contracting mild COVID-19, he presented four times with exertional dyspnea and a thorax computer tomography angiography (CTA) on two occasions and one perfusion scintigraphy revealed no embolism. Based on his high D-dimer values, his symptoms and his history of PE, he was placed on prolonged PE prophylaxis, which was stopped 33 days ago, and at that time, CTA revealed extensive bilateral PE. In conclusion, an unusually longer activation in COVID-19 coagulopathy may co-exist in patients with a history of previous PE, ongoing symptoms and increased D-dimer levels, irrespective of the COVID-19 severity.

6.
Crit Care Explor ; 2(6): e0140, 2020 Jun.
Article in English | MEDLINE | ID: covidwho-1795098

ABSTRACT

OBJECTIVES: To describe a case of acute limb ischemia caused by arterial thrombosis due to coronavirus disease 2019. DESIGN: Clinical observation of a patient. SETTING: Academic medical center. PATIENT: A 59-year-old female with history of hypertension, hyperlipidemia, and prior smoking. INTERVENTION: Clinical observation and data extraction from electronic medical records. MEASUREMENTS AND MAIN RESULTS: We report a case of peripheral arterial thrombosis associated with coronavirus disease 2019, resulting in acute limb ischemia of the right lower extremity. This event was heralded by a sudden and significant elevation in d-dimer levels. At the time of surgery, a long, gelatinous clot was retrieved from the right popliteal artery. Perioperatively, she continued to have absent pedal Doppler signals and after multiple embolectomy attempts, required distal arterial cut down with removal of additional thrombi and resultant improvement of distal arterial flow. CONCLUSIONS: This case demonstrates the importance of regularly checking d-dimer levels and vigilant monitoring for arterial thrombotic events, as they can rapidly become catastrophic.

7.
World J Virol ; 11(2):104-106, 2022.
Article in English | PubMed | ID: covidwho-1791989

ABSTRACT

N-acetyl cysteine (NAC) is a promising drug for prophylaxis and treatment of coronavirus disease 2019 (COVID-19) based on antioxidant and anti-inflammatory mechanisms. Further studies with cautious approach are needed to establish the benefits and risks before considering NAC as an adjuvant treatment for COVID-19.

8.
Indian J Hematol Blood Transfus ; : 1-11, 2021 Aug 19.
Article in English | MEDLINE | ID: covidwho-1782978

ABSTRACT

Covid-19 pandemic reveals that the virus causes Covid-19 associated coagulopathy and it is well known that thrombotic risk is associated with ethnicity. To describe the Covid-19 associated coagulopathy in Indian population and to correlate it with the disease severity and survivor status. A cross sectional descriptive study of 391 confirmed Covid-19 cases was carried out over a period of 1.5 months. Patients were categorised as mild to moderate, severe and very severe and also labelled as survivors and non survivors. Prothrombin time (PT), International normalised ratio (INR), activated partial thromboplastin time, D dimer, Fibrin degradation products (FDP), fibrinogen and thrombin time and platelet counts were investigated among the subgroups. Mean age was higher in patients with severe disease (57.62 ± 13.08) and among the non survivors (56.54 ± 12.78). Statistically significant differences in D dimer, FDP, PT, INR and age were seen among the 3 subgroups and survivors. Strong significant positive correlation was noted between D dimer and FDP (r = 0.838, p < .001), PT and INR (r = 0.986, p < 0.001). D dimer was the best single coagulation parameter as per the area under curve (AUC: 0.762, p < 0.001) and D dimer + FDP was the best combination parameter (AUC: 0.764, p = 0) to differentiate mild moderate from severe disease. Raised levels of D dimer, FDP, PT, PT INR and higher age correlated positively with disease severity and mortality in Indian Population.

9.
Elife ; 112022 03 23.
Article in English | MEDLINE | ID: covidwho-1786253

ABSTRACT

Coagulopathy is a significant aspect of morbidity in COVID-19 patients. The clotting cascade is propagated by a series of proteases, including factor Xa and thrombin. While certain host proteases, including TMPRSS2 and furin, are known to be important for cleavage activation of SARS-CoV-2 spike to promote viral entry in the respiratory tract, other proteases may also contribute. Using biochemical and cell-based assays, we demonstrate that factor Xa and thrombin can also directly cleave SARS-CoV-2 spike, enhancing infection at the stage of viral entry. Coagulation factors increased SARS-CoV-2 infection in human lung organoids. A drug-repurposing screen identified a subset of protease inhibitors that promiscuously inhibited spike cleavage by both transmembrane serine proteases and coagulation factors. The mechanism of the protease inhibitors nafamostat and camostat may extend beyond inhibition of TMPRSS2 to coagulation-induced spike cleavage. Anticoagulation is critical in the management of COVID-19, and early intervention could provide collateral benefit by suppressing SARS-CoV-2 viral entry. We propose a model of positive feedback whereby infection-induced hypercoagulation exacerbates SARS-CoV-2 infectivity.


Subject(s)
COVID-19 , SARS-CoV-2 , Blood Coagulation Factors , Humans , Spike Glycoprotein, Coronavirus , Virus Internalization
10.
Cardiovasc Hematol Agents Med Chem ; 2022 Apr 05.
Article in English | MEDLINE | ID: covidwho-1779862

ABSTRACT

Recently, the post-COVID neurological syndrome has been coined, which describes the functional and structural sequelae of coronavirus infection disease-19 (COVID-19) in the brain. Mild/severe manifestations of the post-COVID neurological syndrome have been identified in approximately 33.00% of COVID-19 survivors. The presence of neurological complications after COVID allowed neuropathologists to investigate in-depth the role of viral infection in neurons. The pathophysiology of the post-COVID neurological syndrome involved the development of a systematic response, including coagulopathy characterized by the formation of microthrombi. Coagulopathy, an old term for a new disease, describes the discrepancy between pro-coagulant and anticoagulant systems due to overexpression of pro-coagulant substances and or their receptors in addition to suppression of the anticoagulant molecules and or their receptors. Vascular endothelial cells and hepatocytes play a central role in the regulation of hemostasis that is disrupted during the acute phase response (APR) of coronavirus-19 (COVID-19). Currently, coagulopathy and inflammation are termed together since both form a complementary system, indicated by the elevation of inflammatory biomarkers (APR) and fibrinolysis biomarkers (D-dimer/fibrin). The later events of post-COVID neurological syndrome are primarily induced by coagulopathy and direct viral tropism. Therefore, the paper introduces the hypothesis of coagulopathy induced post-COVID neurological syndrome.

11.
Front Cardiovasc Med ; 9: 794092, 2022.
Article in English | MEDLINE | ID: covidwho-1775650

ABSTRACT

Introduction: Coagulation parameters are important determinants for COVID-19 infection. We conducted meta-analysis to assess the association between early hemostatic parameters and infection severity. Methods: Electronic search was made for papers that addressed clinical characteristics of COVID-19 patients and disease severity. Results were filtered using exclusion and inclusion criteria and then pooled into a meta-analysis to estimate the standardized mean difference (SMD) with 95% confidence interval (CI) for D-dimers, fibrinogen, prothrombin time, platelet count (PLT), activated partial thromboplastin time. To explore the heterogeneity and robustness of our fundings, sensitivity and subgroup analyses were conducted. Publication bias was assessed with contour-enhanced funnel plots and Egger's test by linear regression. Coagulation parameters data from retrospective cohort study of 451 patients with COVID-19 at National Research Center for Cardiac Surgery were included in meta-analysis of published studies. Results: Overall, 41 original studies (17,601 patients) on SARS-CoV-2 were included. For the two groups of patients, stratified by severity, we identified that D-dimers, fibrinogen, activated partial thromboplastin time, and prothrombin time were significantly higher in the severe group [SMD 0.6985 with 95%CI (0.5155; 0.8815); SMD 0.661 with 95%CI (0.3387; 0.9833); SMD 0.2683 with 95%CI (0.1357; 0.4009); SMD 0.284 with 95%CI (0.1472; 0.4208)]. In contrast, PLT was significantly lower in patients with more severe cases of COVID-19 [SMD -0.1684 with 95%CI (-0.2826; -0.0542)]. Neither the analysis by the leave-one-out method nor the influence diagnostic have identified studies that solely cause significant change in the effect size estimates. Subgroup analysis showed no significant difference between articles originated from different countries but revealed that severity assessment criteria might have influence over estimated effect sizes for platelets and D-dimers. Contour-enhanced funnel plots and the Egger's test for D-dimers and fibrinogen revealed significant asymmetry that might be a sign of publication bias. Conclusions: The hemostatic laboratory parameters, with exception of platelets, are significantly elevated in patients with severe COVID-19. The two variables with strongest association to disease severity were D-dimers and fibrinogen levels. Future research should aim outside conventional coagulation tests and include analysis of clotting formation and platelet/platelet progenitors characteristics.

12.
Tromboz, Gemostaz i Reologiya ; 2021(3):4-11, 2021.
Article in Russian | Scopus | ID: covidwho-1776791

ABSTRACT

Von Willebrand factor (vWF) is a multimeric glycoprotein that plays a key role in platelet and plasma hemostasis. In recent years, the involvement of vWF in angiogenesis, apoptosis of normal and tumor cells has been revealed, and its transport role has been determined. The complex of vWF and enzyme ADAMTS-13, which is responsible for its splitting, is essential in the development of inflammatory processes. The mechanisms of vWF participation in inflammatory processes varies and include inter-action with microorganisms, blood cells and their degradation products, neutrophil extracellular traps, the complement system, etc. The unique qualities of the vWF contribute to the development and progression of coagulopathy in sepsis. Systemic inflammation enhances local inhibition of vWF cleavage and exacerbates an imbalance in the vWF/ADAMTS-13 ratio, which contributes to the development of intravascular coagulation. The formation of ultralarge vWF (ULvWF) multimers and ADAMTS-13 deficiency were detected in sepsis, severe COVID-19, craniocerebral and concomitant trauma, acute kidney injury, etc. The pathogenesis of the resulting multiple organ failure due to the accumulation of ULvWF is based on the development of microangiopathy and micro-vascular thrombosis. Possible methods for correcting disorders in the vWF/АDAMTS-13 system are the use of therapeutic plasma exchange, heparin, N-acetylcysteine, recombinant ADAMTS-13, and magnesium preparations. © Lyanguzov A. V., Sergunina O. Yu., Ignatyev S. V., Kovtunova M. E., Kalinina S. L., Semakin A. S., 2021 © Gemostaz i Reologia LLC, 2021.

13.
Respiration ; : 1-8, 2022 Apr 05.
Article in English | MEDLINE | ID: covidwho-1775042

ABSTRACT

OBJECTIVE: The aim of this study was to investigate the association between serological biomarkers at the acute phase of infection at hospital admission with the development of long-term post-COVID fatigue and dyspnea. METHODS: A cohort study including patients hospitalized due to COVID-19 in one urban hospital of Madrid (Spain) during the first wave of the outbreak (from March 20 to June 30, 2020) was conducted. Hospitalization data, clinical data, and eleven serological biomarkers were systematically collected at hospital admission. Patients were scheduled for an individual telephone interview after hospital discharge for collecting data about the presence of post-COVID fatigue and dyspnea. RESULTS: A total of 412 patients (age: 62 years, standard deviation: 15 years; 47.5% women) were assessed with a mean of 6.8 and 13.2 months after discharge. The prevalence of post-COVID fatigue and dyspnea was 72.8% and 17.2% at 6 months and 45.4% and 13.6% at 12 months after hospital discharge, respectively. Patients exhibiting post-COVID fatigue at 6 or 12 months exhibited a lower hemoglobin level, higher lymphocyte count, and lower neutrophil and platelets counts (all, p < 0.05), whereas those exhibiting post-COVID dyspnea at 6 or 12 months had a lower platelet count and lower alanine transaminase, aspartate transaminase, and lactate dehydrogenase (LDH) levels (all, p < 0.05) than those not developing post-COVID fatigue or dyspnea, respectively. The multivariate regression analyses revealed that a lower platelet count and lower LDH levels were associated but just explaining 4.5% of the variance, of suffering from post-COVID fatigue and dyspnea, respectively. CONCLUSION: Some serological biomarkers were slightly different in patients exhibiting post-COVID fatigue or dyspnea, but they could not explain the long-COVID problems in those patients.

14.
Blood ; 138(SUPPL 1):1045, 2021.
Article in English | EMBASE | ID: covidwho-1770423

ABSTRACT

Objective: Identify a plasma-based activity, or biomarker, that defines the mechanism(s) by which Covid-19 disease triggers excessive coagulation. Introduction: While acute respiratory syndrome is the fundamental feature of severe Covid-19 disease, having a high level of the coagulation biomarker D-dimer upon admission is associated with increased thrombosis and mortality. As such, hospitalized patients are often placed on anticoagulant heparins. How Covid-19 triggers excessive coagulation is unresolved. Sars-CoV-2 infection could expose existing tissue factor (TF) to blood or, via cytokines, induce TF expression on cells that are in direct contact with blood. Extracellular vesicles (EV) are lipid bound microparticles released by all types of healthy and damaged cell and Covid-19 patient plasma EV TF activity has been recently reported. Cellular activation and damage due to SARS-CoV-2 could also release polyanionic nucleic acids and polyphosphates and generate neutrophil extracellular traps as contact surfaces for clot formation. Methods: Study 1. We attempted to identify excessive coagulation pathway activities in Covid-19 plasma-based, Ca++-induced thrombin generation assays. Assays were performed in the absence and presence of selective extrinsic (TF) and intrinsic (contact activation) pathway inhibitors (n=296 plasma samples). D-dimer levels were also determined. In a smaller study, Covid-19 patient samples were collected directly into citrate or citrate plus corn trypsin inhibitor, then processed for analysis. Study 2. We conducted studies to evaluate the extent to which EV TF activity contributes to the Covid-19-associated coagulopathies. Plasma EVs were isolated and EV TF activity determined by the difference in FXa activity in the absence vs presence of anti-TF antibody. D-dimer and tissue factor pathway inhibitor a (TFPIa) antigen levels were measured. Data from 232 samples collected from 96 Covid-19 positive patients and 18 samples from 14 healthy controls were analyzed. For each study analysis, patient samples were organized into groups based on the disease severity outcomes as follows: hospitalization (Hospitalization;n=37);intensive care (ICU;n=16);mechanical ventilation (Ventilation;n=22);or fatality (Deceased;n=22). Result: Study 1. Covid-19 samples showed considerable thrombin generation variability with some samples failing to generate thrombin;pathway selective inhibitors reduced thrombin generation while heparinase treatment increased thrombin generation. Upon analysis, thrombin generation parameters showed no significant correlations to either D-dimer levels or disease severity. Instead, plasma prepared from blood collected directly into corn trypsin inhibitor revealed that contact activation that occurred post-sample collection dominates procoagulant activity. Study 2. Figure 1, shows EV TF activities, D-dimer and TFPIα levels obtained for Covid-19 samples, with data segregated based on disease severity outcomes. Statistically significant difference versus the Hospitalized group are shown. TFPIa levels were highest in heparin IV patients (24.4+1.5 nM) vs Heparin-SQ (12.8+0.9 nM) vs enoxaparin (10.8 +0.7 nM) (p value:<0.0001). It is known that heparin treatment increases circulating TFPIα, however an increase in TFPIα might also further increase circulating TF/FVIIa/XaTFPI inhibitory complex, which would dissociate in citrated plasma, and might account for the increase in EV TF in other studies. Conclusions: Contact activation that occurs post-sample collection is sufficient to obscure endogenous triggers of coagulation, if present, in Covid-19 patients' plasma. D-dimer and TFPIα strongly correlate with disease severity although the latter is likely affected by heparin treatment. The most severe Covid-19 patients with high D-dimer did not show detectible plasma EV TF activity. Plasma EV TF activity does not appear to adequately represent the mechanism responsible for elevated D-dimer levels in Covid-19 cases.

15.
European Heart Journal, Supplement ; 23(SUPPL F):F7, 2021.
Article in English | EMBASE | ID: covidwho-1769250

ABSTRACT

Background and Aims: The use of therapeutic anticoagulation to improve outcomes in COVID-19-associated coagulopathy remains unclear. We aimed to compare the efficacy and safety of therapeutic versus standard prophylactic anticoagulation in this population. Methods and Results: This was a single-center, open-label, two-arms, randomized controlled study conducted from 1st April to 15th July 2021. Two-hundred fifty severe COVID-19 patients with coagulopathy were randomly assigned (1:1 ratio) to receive either prophylactic anticoagulation (subcutaneous unfractionated heparin/UFH 5000IU b.i.d or fondaparinux 2.5mg o.d) or therapeutic anticoagulation (weightadjusted dose UFH or fondaparinux). Anticoagulation was administered until hospital discharge or at the treating physician's discretion. All patients received international COVID-19 guideline-driven therapy throughout the study. Baseline characteristics were not significantly different (p>0.05) between both arms, except for the Ddimer and CRP level at admission (p=0.04;p=0.001;respectively). During a 30-day follow-up, therapeutic arm revealed significant higher need for NIV/invasive MV (41.3% vs. 29%, p=0.02), higher progression to ARDS (34.1% vs. 16.1%, p=0.001), and increased 30-day all-cause mortality (58.7% vs. 15.3%, p<0.001) as compared with prophylactic arm. There was no significant difference between both arms in the incidence of acute MI (20% vs. 13.6%, p=0.07), VTE (4.8% vs. 0.8%, p=0.09), arterial thromboembolism (3.2% vs. 0%, p=0.29) and overall bleeding (17.6% vs. 6.4%, p=0.18) at 30-days. Conclusion: Therapeutic anticoagulation was considered safe and effective in preventing thromboembolic events, but not in the need for NIV/invasive MV, progression to ARDS and 30-day all-cause mortality in hospitalized patients with severe COVID-19 and coagulopathy.

16.
Cureus ; 14(2): e22061, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1766139

ABSTRACT

Background Studies suggest that COVID-19 infection may induce increased hypercoagulability, leading to thrombotic complications. The high rates of thrombotic complications among patients receiving standard-dose deep venous thrombosis (DVT) prophylaxis have prompted some clinicians to support the empiric increase of anticoagulation (AC) doses used for prophylaxis in patients with COVID-19. At present, the optimal anticoagulant agents, dosages, and duration have not been designated. We conducted a retrospective study to assess for outcomes in patients who received treatment for COVID-19 based on various dosings of AC. Methods This was a single-institution, retrospective cross-sectional study including patients with a positive COVID-19 test who were admitted within the St. Joseph's Health Network from September to November of 2020. The inclusion criteria were men and women aged 18 years or older who had confirmed COVID-19 by polymerase chain reaction (PCR). Medical charts of patients who met the inclusion criteria were audited to obtain information. The patients were separated into three cohorts: those who received DVT prophylactic dose of AC, those who received an intermediate dose of AC, and those who received therapeutic AC. Results A total of 440 patients were included in the study, of whom 236 were Hispanic (50.3%), 131 were Caucasian (27.1%), 47 were African American (10.7%), and 26 were Asian (5.9%). The most common comorbidities were hypertension (273/440 [62.2%]), diabetes 189/440 [43.1%]), and coronary artery disease (60/440 [13.7%]). In the DVT prophylactic dose of AC cohort, there were 215 patients, and the average length of stay was 10.3 days. Eleven patients experienced bleeding events, five patients experienced thrombotic events, 16 patients required mechanical ventilation, and 20 patients died. In the intermediate dose of AC cohort, there were 63 patients, and the average length of stay was 10.3 days. Three patients experienced bleeding events, two patients experienced thrombotic events, seven patients required mechanical invasive ventilation, and 11 patients died. In the therapeutic dose of AC cohort, there were 162 patients, and the average length of stay was 14 days. In this cohort, 19 patients experienced bleeding events, 12 patients experienced thrombotic events, 26 patients required invasive mechanical ventilation, and 29 patients died. Patients who received intermediate dosing of AC also had the lowest risk of thrombotic events (0.05). Patients who received intermediate dosing of AC had the lowest rates of requiring both high-flow nasal cannula (p = 0.0001) and invasive mechanical ventilation (p = 0.031). Patients who received intermediate dosing of AC had a lower rate of bleeding compared to those who received the DVT prophylaxis dose and systemic AC dose (p = 0.037). The DVT prophylactic and intermediate dosing of AC groups had a shorter length of stay in comparison to the systemic AC group (p = 0.0002). Conclusion In comparison to the venous thromboembolism prophylaxis dose and systemic AC dose groups, intermediate dosing of AC had the lowest rates of hemorrhage, mortality, length of stay, and requirement of high-flow nasal cannula or mechanical invasive ventilation. In the systemic dose AC group, there were worse clinical outcomes in terms of length of stay, incidence of bleeding events, requirement of mechanical ventilator use, and rate of mortality.

17.
Int J Mol Sci ; 23(6)2022 Mar 19.
Article in English | MEDLINE | ID: covidwho-1760654

ABSTRACT

Coronavirus Disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is frequently complicated by thrombosis. In some cases of severe COVID-19, fibrinolysis may be markedly enhanced within a few days, resulting in fatal bleeding. In the treatment of COVID-19, attention should be paid to both coagulation activation and fibrinolytic activation. Various thromboses are known to occur after vaccination with SARS-CoV-2 vaccines. Vaccine-induced immune thrombotic thrombocytopenia (VITT) can occur after adenovirus-vectored vaccination, and is characterized by the detection of anti-platelet factor 4 antibodies by enzyme-linked immunosorbent assay and thrombosis in unusual locations such as cerebral venous sinuses and visceral veins. Treatment comprises high-dose immunoglobulin, argatroban, and fondaparinux. Some VITT cases show marked decreases in fibrinogen and platelets and marked increases in D-dimer, suggesting the presence of enhanced-fibrinolytic-type disseminated intravascular coagulation with a high risk of bleeding. In the treatment of VITT, evaluation of both coagulation activation and fibrinolytic activation is important, adjusting treatments accordingly to improve outcomes.


Subject(s)
Blood Coagulation Disorders/etiology , COVID-19 Vaccines/adverse effects , COVID-19/complications , SARS-CoV-2 , Biomarkers , Blood Coagulation , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/prevention & control , Blood Coagulation Disorders/therapy , Blood Coagulation Tests , COVID-19/immunology , COVID-19/prevention & control , COVID-19 Vaccines/immunology , Combined Modality Therapy , Disease Management , Disease Susceptibility , Fibrinolysis , Humans , Prognosis , Treatment Outcome
18.
Front Neurol ; 13: 834469, 2022.
Article in English | MEDLINE | ID: covidwho-1753393

ABSTRACT

Background: Acute ischemic stroke (AIS) is a possible complication of coronavirus disease 2019 (COVID-19) infection. Although peculiar clinical features and underlying specific mechanisms of thrombogenesis have been suggested so far, there is no consensus on the appropriate vascular preventive drug regimen in patients with COVID-19. Aim and Methods: From a larger clinical series of consecutive acute ischemic strokes related to COVID-19 admitted to three cerebrovascular units in Northern Italy, herein, we describe the clinical features of a subgroup of patients in whom stroke occurred despite therapeutic anticoagulation. Results: A total of seventeen/80 AIS related to COVID-19 (21.2%) occurred in anticoagulated patients. Although no blood level was available for Direct Oral AntiCoagulant, the drug dosage was appropriate according to guidelines. Their National Institute of Health Stroke Scale (NIHSS) at admission was 12.0 (SD = 7.4) and 58.8% of them had evidence of large vessel occlusion. The case fatality rate was as high as 64.7%. Discussion and Conclusions: The occurrence of an anticoagulation failure seems to be increased in the setting of COVID-19 infection, with worse clinical outcomes if compared to non-COVID-19 related ischemic strokes. We discuss the diagnostic and therapeutic implications of such evidence, suggesting that some arterial thrombotic complications might be either resistant to or independent of the anticoagulation effect.

19.
Front Cell Infect Microbiol ; 12: 807332, 2022.
Article in English | MEDLINE | ID: covidwho-1753361

ABSTRACT

In the early stage of coronavirus disease 2019 (COVID-19), most cases are identified as mild or moderate illnesses. Approximately 20% of hospitalised patients become severe or critical at the middle or late stage of the disease. The predictors and risk factors for prognosis in those with mild or moderate disease remain to be determined. Of 694 patients with COVID-19, 231 patients with mild or moderate disease, who were hospitalised at 10 hospitals in Wenzhou and nearby counties in China, were enrolled in this retrospective study from 17 January to 20 March 2020. The outcomes of these patients included progression from mild/moderate illness to severe or critical conditions. Among the 231 patients, 49 (21.2%) had a poor prognosis in the hospital. Multivariate logistic regression analysis showed that higher inflammation/coagulopathy/immunology responsive index (ICIRI=[c-reactive protein × fibrinogen × D-dimer]/CD8 T cell count) on admission (OR=345.151, 95% CI=23.014-5176.318) was associated with increased odds ratios for poor prognosis. The area under the receiver operating characteristic curve for ICIRI predicting severe and critical condition progression was 0.65 (95% CI=0.519-0.782) and 0.80 (95% CI=0.647-0.954), with cut-off values of 870.83 and 535.44, respectively. Conversely, age, sex, comorbidity, neutrophil/lymphocyte ratio, CD8 T cell count, and c-reactive protein, fibrinogen, and D-dimer levels alone at admission were not good predictors of poor prognosis in patients with mild or moderate COVID-19. At admission, a novel index, ICIRI, tends to be the most promising predictor of COVID-19 progression from mild or moderate illness to severe or critical conditions.


Subject(s)
Blood Coagulation Disorders/virology , COVID-19 , Inflammation/virology , C-Reactive Protein , CD8-Positive T-Lymphocytes/immunology , COVID-19/complications , COVID-19/diagnosis , COVID-19/immunology , Fibrin Fibrinogen Degradation Products , Fibrinogen , Humans , ROC Curve , Retrospective Studies
20.
Open Forum Infectious Diseases ; 8(SUPPL 1):S277, 2021.
Article in English | EMBASE | ID: covidwho-1746648

ABSTRACT

Background. COVID 19 is associated with a hypercoagulable state with cytokine storm syndrome and thrombocytopenia leading to complications across various systems. COVID-19 infection, its treatment, resultant immunosuppression, and pre-existing comorbidities have made patients vulnerable to secondary infections Methods. We systematically reviewed COVID-19 cases between Jan to May 2021 for pulmonary and extrapulmonary complications. Patients with recent COVID-19 vaccination and neurological symptoms were also included. Results. Neurological complications: Neurological complications include ischemic and haemorrhagic strokes. Other complications are encephalopathy, encephalitis, Guillain-Barré syndrome, acute hemorrhagic necrotizing encephalopathy. Demyelination and radiculopathies are seen as post vaccination complications. Mucormycosis: Unprecedented high rate of invasive fungal sinusitis in association with COVID -19 is reported from the Indian subcontinent. This has a propensity for intra orbital and intracranial extension. COVID -19 associated coagulopathy: COVID -19 is a pro-inflammatory hypercoagulable state. Pulmonary thromboembolism, deep venous thrombosis and catheter related thrombosis are well documented. Cardiac complications: Cardiac manifestations include Myocardial Injury with non-obstructed coronary arteries (MINOCA), myocarditis, myocardial ischemia, cardiomyopathy. Pulmonary complications and sequelae of COVID -19: Progression of lung injury to ARDS during the initial phase and fibrosis of parenchyma in the recovery phase. Spontaneous pneumomediastinum, pneumatoceles and pneumothorax and secondary infections are identified in our study. COVID- 19 associated gastrointestinal complications: Patients evaluated for renal colic, pancreatitis, cholecystitis showed, ground glass opacities or subpleural bands in typical Covid-19 distribution. COVID-19 may lead of acute kidney and bowel injury due to arterial thrombosis. COVID - 19 associated myonecrosis: Ischemia of the small caliber vessels may result in myonecrosis. Conclusion. Awareness of these unusual manifestations will facilitate an early diagnosis, improve management and help reduce morbidity and mortality.

SELECTION OF CITATIONS
SEARCH DETAIL