scholarly journals COVID-19 Disease and Hypercoagulability Leading to Acute Ischemic Stroke

2020 ◽  
pp. 194187442096032
Author(s):  
Naresh Mullaguri ◽  
Madihah Hepburn ◽  
James Matthew Gebel ◽  
Ahmed Itrat ◽  
Pravin George ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Ischemic Stroke ◽  
Respiratory Failure ◽  
Acute Phase ◽  
Case Series ◽  
Disease Case ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic ◽  
Exposure Risks ◽  
Cerebral Ischemic

Introduction: SARS-Coronavirus-2 infection leading to COVID-19 disease presents most often with respiratory failure. The systemic inflammatory response of SARS-CoV-2 along with the hypercoagulable state that the infection elicits can lead to acute thrombotic complications including ischemic stroke. We present 3 cases of patients with COVID-19 disease who presented with varying degrees of vascular thrombosis. Cases: Cases 1 and 2 presented as cerebral ischemic strokes without respiratory failure. Given their exposure risks, they were both tested for COVID-19 disease. Case 2 ultimately developed respiratory failure and pulmonary embolism. Cases 2 and 3 were found to have simultaneous arterial and venous thromboembolism (ischemic stroke and pulmonary embolism) as well as positive antiphospholipid antibodies. Conclusion: Our case series highlight the presence of hypercoagulability as an important mechanism in patients with COVID-19 disease with and without respiratory failure. Despite arterial and venous thromboembolic events, antiphospholipid and hypercoagulable panels in the acute phase can be difficult to interpret in the context of acute phase response and utilization of thrombolytics. SARS-CoV-2 testing in patients presenting with stroke symptoms may be useful in communities with a high case burden or patients with a history of exposure.

scholarly journals Venous tromboembolic complications in stroke

2018 ◽  
pp. 70-77
Author(s):  
Екатерина Владимировна Силина ◽  
Е.Н. Кабаева ◽  
В.А. Ступин ◽  
А.А. Тяжельников ◽  
Т.Г. Синельникова ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Hemorrhagic Stroke ◽  
Clinical Laboratory ◽  
Disease Onset ◽  
Test Results ◽  
Thromboembolic Complications ◽  
Severe Stroke ◽  
Laboratory Markers ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic

Актуальность работы обусловлена поиском путей улучшения результатов лечения больных инсультом. Цель исследования: выявить критерии прогноза риска развития венозных тромбозов, а также ключевые звенья патогенеза тромбоэмболических осложнений у пациентов с острым инсультом. Материалы и методы: в проспективное исследование включено 145 больных с инсультом (104 с ишемическим (ИИ) и 41 с геморрагическим (ГИ)), госпитализированных в отделение нейрореанимации в период 3,5-24 часа от начала заболевания и имеющих на момент включения в исследование различную степень депрессии сознания (тяжелая степень инсульта). Пациентам проводилась терапия в соответствии со стандартами оказания медицинской помощи, согласно которым всем пациентам назначали антикоагулянтную терапию (АКТ). Выполняемый в динамике стандартный клинико-диагностический и лабораторный мониторинг был дополнен тестом «Тромбодинамика». Результаты: у 95% пациентов с инсультом зарегистрированы различные факторы риска венозных тромбоэмболических осложнений (ВТЭО). Тромбоэмболия легочной артерии (ТЭЛА) развилась в 24% случаев, преимущественно на 2-3 неделе, в среднем через 6 дней после отмены АКТ. Описана динамика и признаки дисбаланса в системе гемостаза у больных инсультом, нараставшие после отмены АКТ. Показано, что стандартные методы исследования системы гемостаза по сравнению с прямым методом менее информативны для выявления ВТЭО и оценки эффективности АКТ. Вероятность развития ВТЭО прямо пропорциональна скорости смены состояния гиперкоагуляции состоянием гипокоагуляции. При этом состояние фоновой гиперкоагуляции не коррелирует с развитием ВТЭО. Корреляционный анализ изменений в системе гемостаза с динамикой клинико-лабораторных маркеров у больных с тяжелым инсультом выявил закономерные изменения показателей коагуляционного гемостаза в условиях реализации разных схем стандартной АКТ. Эти схемы были сопоставимы по содержанию при развитии как ВТЭО и ТЭЛА, так и геморрагических осложнений. Вывод: К больным инсультом необходим персонализированный подход при динамическом мониторировании гемостаза и назначении антикоагулянтной терапии. This work was warranted by the need to improve results in the treatment of stroke. The aim of this study was to identify criteria for predicting the risk of venous thrombosis and to elucidate the pathogenesis of thromboembolic complications in patients with acute stroke. Materials and methods. This prospective study included 145 patients (104 patients with ischemic stroke and 41 patients (28.3%) with hemorrhagic stroke). All patients were hospitalized to the neuroresuscitation unit within 3.5 to 24 hours of the disease onset at different stages of consciousness impairment. The patients received anticoagulant therapy (ACT) according to current healthcare standards. Standard clinical diagnostic and laboratory monitoring was supplemented with a Thrombodynamics test. Results. Risk factors for venous thromboembolic events (VTE) were observed in 95% of patients. Pulmonary embolism developed in 24% of cases mostly during weeks 2-3, generally at 6 days of ACT withdrawal. Hemostatic changes and disbalance progressed after the ACT withdrawal. Standard methods of studying hemostasis were shown to be less informative in detecting VTE and evaluating ACT efficacy than the thermodynamics method. The probability of VTE was directly proportional to the velocity of hypercoagulation transformation into hypocoagulation. In this process, the background hypocoagulation was not correlated with the development of VTE. Analysis of correlations of hemostasis changes with changes in clinical-laboratory markers identified relationships of changes in coagulation hemostasis with different standard ACT programs. VTE, pulmonary embolism, and hemorrhagic complications developed in association with administration of comparable ACT programs to patients with severe stroke.

Abstract P673: The Obesity Paradox in Patients Hospitalized for Ischemic Stroke

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Genaro Velazquez ◽  
Hafeez Shaka ◽  
Hernan G. Marcos-Abdala ◽  
Emmanuel Akuna
Keyword(s):  
Pulmonary Embolism ◽  
Risk Factor ◽  
Ischemic Stroke ◽  
Respiratory Failure ◽  
Hospital Mortality ◽  
Odds Ratio ◽  
Mechanical Thrombectomy ◽  
Length Of Hospital Stay ◽  
Obesity Paradox ◽  
Secondary Outcomes

Introduction: Even though Obesity, as measured by BMI > 30.00 kg/m 2 , is a established risk factor for ASCVD, it hasn’t been proven as a risk factor for adverse outcomes in patients with diagnosis of ischemic stroke. Our study sought to compare outcomes for ischemic stroke hospitalizations in patients with and without Obesity. Methods: A retrospective cohort study was conducted using the Nationwide Inpatient Sample from 2016 and 2017. About 71,473,874who had ischemic stroke as primary diagnosis were enrolled and further stratified based on the presence or absence of Obesity as secondary diagnosis using ICD-10 codes. The primary outcome was inpatient mortality and secondary outcomes included length of hospital stay, treatment with mechanical thrombectomy, treatment with tPA, and complications like respiratory failure requiring intubation, pulmonary embolism (PE), DVT, NSTEMI and sepsis. Multivariate regression analysis was done to adjust for confounders. Results: The in-hospital mortality for patients with ischemic stroke was 42 145 overall. Compared with patients without obesity, patients with Obesity had a lower odds of in- hospital mortality (aOR 0.85, 95% CI 0.79-0.93, p<0.001) when adjusted for patient and hospital characteristics. We found that patients with ischemic stroke and obesity had decreased length of hospital stay and higher odds ratio of treatment with mechanical thrombectomy, treatment with tPA, and higher odds ratio of complications like respiratory failure requiring intubation and pulmonary embolism (PE). No significant difference in other secondary outcomes (DVT, NSTEMI and sepsis). Conclusion: There is convincing evidence supporting the existence of the “obesity paradox” in patients with ischemic stroke. Several stroke-associated mechanisms, like autonomous nervous activation and pro-inflammatory cytokine release in addition to other factors like impaired feeding and inactivity cause accelerated tissue degradation and overall weight loss. It is thought that obese patients with better metabolic reserve may be less affected from this unfavorable metabolic dysregulation as compared to underweight patients. Nevertheless, further studies are needed in order to identify factors responsible for this paradox.

scholarly journals Pulmonary Embolism and Severe Asthma: Case Report and Literature Review

Medicina ◽  
2019 ◽  
Vol 55 (10) ◽  
pp. 647 ◽  
Author(s):  
Lee ◽  
Fu
Keyword(s):  
Pulmonary Embolism ◽  
Severe Asthma ◽  
Inflammatory Diseases ◽  
Severe Disease ◽  
Plasminogen Activator Inhibitor ◽  
Cell Types ◽  
Massive Pulmonary Embolism ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic ◽  
Activator Inhibitor Type

Pulmonary embolism is a life-threatening disease. Its development is generally thought to be due to causes collectively known as the Virchow's triad. Chronic inflammations are associated with the activation of coagulation and increased risks of venous thromboembolic events. Asthma is one of the chronic inflammatory diseases associated with procoagulants and antifibrinolytic activities in the airways. Coagulation is activated in patients with asthma with the following steps of pathophysiology: Increased tissue factor expression in various cell types, decreased activity of the anticoagulant protein C system and inhibition of fibrinolysis through over-production of plasminogen activator inhibitor type 1 (PAI-1). Asthma is therefore likely a risk factor for pulmonary embolism, especially in those patients with severe disease conditions together with frequent exacerbation. Here we present a case of severe asthma associated with coagulopathy and complicated by massive pulmonary embolism, presented with typical S1Q3T3 on electrocardiography (ECG) and massive thrombosis on computed tomography angiography, successfully treated with directed catheter thrombolytic therapy.

High incidence of in-hospital pulmonary embolism following joint arthroplasty with dalteparin prophylaxis

2010 ◽  
Vol 103 (01) ◽  
pp. 123-128 ◽  
Author(s):  
Jason Kerr ◽  
Lori-Ann Linkins
Keyword(s):  
Pulmonary Embolism ◽  
Knee Arthroplasty ◽  
Hip Arthroplasty ◽  
Tertiary Care ◽  
Signs And Symptoms ◽  
Joint Arthroplasty ◽  
Vein Thrombosis ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic ◽  
Deep Vein

SummaryThe in-hospital incidence of pulmonary embolism (PE) in patients undergoing elective joint arthroplasty who receive a minimum of 10 days of dalteparin prophylaxis is reported to be less than 1%. Recent clinical experience raised suspicion that the incidence of PE was significantly higher at our tertiary care institution. It was the objective of this study to determine the incidence of in-hospital PE and symptomatic deep-vein thrombosis following elective joint arthroplasty in patients who received a minimum of 10 days of dalteparin prophylaxis. Consecutive charts of patients who underwent elective joint arthroplasty at our institution between January 2008 and June 2008 were reviewed. Data on risk factors for venous thromboembolism, objectively documented venous thromboembolic events, and signs and symptoms of PE were abstracted. Patients who received concomitant warfarin in the postoperative period were excluded. The study population consisted of 437 knee arthroplasty and 246 hip arthroplasty patients. The incidence of in-hospital PE following knee arthroplasty and hip arthroplasty was 4.6% and 0.4%, respectively. One out of every 10 knee patients, and one out of every 20 hip patients underwent testing for pulmonary embolism. Pulmonary embolism was diagnosed a median of 3.5 days after knee arthroplasty. The incidence of in-hospital PE in knee arthroplasty patients who received dalteparin prophylaxis was significantly higher than expected. Potential explanations for this finding include poor efficacy of dalteparin started 12–24 hours postoperatively and/or a low threshold for ordering diagnostic imaging for PE. Studies to clarify these issues are needed.

scholarly journals Systemic Thrombolysis for Treatment of Postpartum Saddle Embolism Complicated by Postpartum Hemorrhage: A Case Report and Brief Literature Review

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Kathy Mostajeran ◽  
Hillary Boswell ◽  
Ziad Haidar
Keyword(s):  
Pulmonary Embolism ◽  
Case Report ◽  
Postpartum Hemorrhage ◽  
Postpartum Period ◽  
Case Series ◽  
Massive Pulmonary Embolism ◽  
Thromboembolic Events ◽  
Systemic Thrombolysis ◽  
Venous Thromboembolic Events ◽  
In Pregnancy

Venous thromboembolic events (VTE), specifically pulmonary embolisms, account for a significant portion of maternal morbidity and mortality. Due to the procoagulant physiological changes that occur, pregnancy and the postpartum period are known risk factors for thromboembolic events. The risk is greatest during the first-week postpartum and remains elevated for up to six weeks as compared to the general population. Treatment guidelines regarding the use of thrombolytics for massive pulmonary embolism occurring in pregnancy and the postpartum are not well established. In nonpregnant populations, thrombolytic agents are well known to decrease the mortality in the setting of a massive pulmonary embolism. However, in the absence of management guidelines, thrombolysis in pregnancy remains guided by case reports and case series. We present a case of a massive pulmonary embolism (PE) causing hemodynamic instability during the postpartum period treated with tissue plasminogen activator (tPA). The case was complicated by delayed postpartum hemorrhage successfully managed with the uterotonic methylergometrine. The patient was started on oral anticoagulation and continued for six months without recurrent VTE. Our case demonstrates a rare occurrence of a saddle embolism after a vaginal delivery within the first postpartum week which was successfully managed with the use of systemic thrombolysis and minimal intervention to manage the iatrogenic delayed postpartum hemorrhage. To the authors’ knowledge, no other similar case report exists. This case highlights the need to develop guidelines for the use of thrombolysis in mothers who present with massive pulmonary embolus and a noninvasive means to manage adverse bleeding events in the puerperium.

Development of Venous Thromboembolic Events in Cancer Patients with Elevated Levels of Tissue Factor-Bearing Microparticles

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3832-3832
Author(s):  
Jeffrey Zwicker ◽  
Howard A. Liebman ◽  
Donna Neuberg ◽  
Kenneth Bauer ◽  
Furie Barbara ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Cancer Patients ◽  
Tissue Factor ◽  
Thrombus Formation ◽  
P Value ◽  
Prospective Clinical Study ◽  
Thromboembolic Events ◽  
Increased Risk ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic

Abstract Cancer cells shed procoagulant vesicles containing tissue factor, and these tissue factor-bearing microparticles (TFMP) may play a role in thrombus formation in vivo. Using impedance-based flow cytometry to quantify microparticles and a high affinity monoclonal antibody specific for tissue factor, we previously demonstrated the presence of tissue factor-bearing microparticles in platelet-poor plasma in cancer patients. In this case control study, tissue factor-bearing microparticles represented a 4-fold risk factor for venous thromboembolic events (VTE) in cancer patients with acute VTE compared to age, stage, sex, diagnosis-matched controls with cancer but without acute VTE. To further assess the relationship between tissue factor-bearing microparticles and VTE, we performed a retrospective analysis of deep venous thrombosis or pulmonary emboli diagnosed in cancer patients initially enrolled without evidence of VTE. All radiographic reports for the cancer-no VTE group in the 2 years following enrollment were analyzed by a reviewer blinded to microparticle status. Only documented evidence of a new proximal extremity deep vein thrombosis or pulmonary embolism was included in the analysis. The TFMP and no-TFMP groups did not differ significantly for age, sex, active cancer treatment, smoking status, diabetes, or the presence of metastatic disease at time of enrollment. Sixteen of the 60 patients in this group had measurable tissue factor-bearing microparticles, 4 (4/16; 25%) of which subsequently developed radiographic evidence of VTE within 12 months of enrollment. No thrombotic events were recorded among the 44 patients without detectable tissue factor-bearing microparticles within the initial 12 months; however, one patient developed a pulmonary embolism 17 months following enrollment. Identifying death without VTE as a competing risk, the one-year estimate of the rate of VTE in cancer patients with detectable tissue factor-bearing microparticles was 34.8%; among the same group without detectable tissue factor-bearing microparticles, the 1-year rate was 0% (Log Rank p-value=0.002). The presence of tissue factor-bearing microparticles in cancer patients initially thrombosis-free predicted a 7-fold increased risk of thrombosis over cancer patients who were negative for tissue factor-bearing microparticles (OR 7.00, 95% CI 0.85–82.74, P=0.02). These tissue factor-bearing microparticles appear to be derived from the underlying malignancy since samples analyzed from patients with pancreatic cancer demonstrated co-expression of both tissue factor and MUC-1, a transmembrane glycoprotein overexpressed in epithelial malignancies. These data further support the role of tissue factor-bearing microparticles in the pathogenesis of cancer-associated thrombosis and as a biomarker for the prediction of cancer patients at risk of thrombosis. A prospective clinical study, currently being initiated, is required to evaluate this biomarker for the prediction of VTE risk in cancer patients and the utility of thromboprophylaxis in patients with elevated numbers of tissue factor-bearing microparticles.

scholarly journals H1N1-Induced Venous Thromboembolic Events? Results of a Single-Institution Case Series

2016 ◽  
Vol 3 (4) ◽  
Author(s):  
Evangelos Dimakakos ◽  
Dimitra Grapsa ◽  
Ioannis Vathiotis ◽  
Aggeliki Papaspiliou ◽  
Meropi Panagiotarakou ◽  
...  
Keyword(s):  
Influenza A ◽  
Case Series ◽  
Thromboembolic Events ◽  
Vein Thrombosis ◽  
Imaging Characteristics ◽  
Influenza A H1n1 ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic ◽  
Deep Vein ◽  
Novel Influenza A

Abstract We describe the clinical and imaging characteristics of 7 cases with polymerase chain reaction-confirmed novel influenza A H1N1 virus (pH1N1) infection who developed venous thromboembolic events (VTEs) while being hospitalized for influenza pneumonia. Pulmonary embolism (PE) without deep vein thrombosis (DVT) was observed in 6 of 7 cases (85.7%); PE with underlying DVT was found in 1 patient (14.3%).

Thromboembolic Events in Children and Young Adults With Pediatric Sarcoma

2007 ◽  
Vol 25 (12) ◽  
pp. 1519-1524 ◽  
Author(s):  
Ido Paz-Priel ◽  
Lauren Long ◽  
Lee J. Helman ◽  
Crystal L. Mackall ◽  
Alan S. Wayne
Keyword(s):  
Pulmonary Embolism ◽  
Young Adults ◽  
Vena Cava ◽  
Thromboembolic Events ◽  
Pediatric Sarcoma ◽  
Increased Risk ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic ◽  
Localized Disease ◽  
Children And Young Adults

Purpose Adults with malignancy are at increased risk for venous thromboembolic events (TEs). However, data in children and young adults with cancer are limited. Patients and Methods To determine the risk and clinical features of TEs in children and young adults with sarcoma, we reviewed records on 122 consecutive patients with sarcoma treated from October 1980 to July 2002. Results Twenty-three TEs were diagnosed in 19 of 122 (16%; 95% CI, 10% to 23%) patients. Prevalence by diagnosis was Ewing sarcoma, eight of 61 (13%); osteosarcoma, two of 20 (10%); rhabdomyosarcoma, four of 26 (15%); and other sarcomas, five of 15 (33%). TEs developed in 23% of patients with metastases at presentation versus 10% with localized disease (odds ratio, 2.59; 95% CI, 0.9 to 7.1; P < .06). Fifty-three percent of patients with thrombosis had a clot at presentation. A lupus anticoagulant was detected in four of five evaluated patients. There was a single fatality due to pulmonary embolism. Patients who were diagnosed with cancer after 1993 had a higher rate of TE (7% v 23%; P < .015). Of the 23 events, 43% were asymptomatic. Main sites of thromboses were deep veins of the extremities (10 of 23; 43%), pulmonary embolism (five of 23; 22%), and the inferior vena cava (four of 23; 17%). TEs were associated with tumor compression in eight of 23 (35%) and with venous catheters in three of 23 (13%). Conclusion Thromboembolism is common in pediatric patients with sarcomas. Thromboses are detected frequently around the time of oncologic presentation, may be asymptomatic, and seem to be associated with a higher disease burden. Children and young adults with sarcoma should be monitored closely for thrombosis.

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