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Hypercoagulability and reduced fibrinolysis are well-established complications associated with COVID-19. However, the timelines for the onset and resolution of these complications remain unclear. The aim of this study was to evaluate, in a cohort of COVID-19 patients, changes in coagulation and fibrinolytic activity through ROTEM assay at different time points during the initial 30 days following the onset of symptoms in both mild and severe cases. Blood samples were collected at five intervals after symptoms onset: 6-10 days, 11-15 days, 16-20 days, 21-25 days, and 26-30 days. In addition, fibrinogen, plasminogen, PAI-1, and alpha 2-antiplasmin activities were determined. Out of 85 participants, 71% had mild COVID-19. Twenty uninfected individuals were evaluated as controls. ROTEM parameters showed a hypercoagulable state among mild COVID-19 patients beginning in the second week of symptoms onset, with a trend towards reversal after the third week of symptoms. In severe COVID-19 cases, hypercoagulability was observed since the first few days of symptoms, with a tendency towards reversal after the fourth week of symptoms onset. A hypofibrinolytic state was identified in severe COVID-19 patients from early stages and persisted even after 30 days of symptoms. Elevated activity of PAI-1 and alpha 2-antiplasmin was also detected in severe COVID-19 patients. In conclusion, both mild and severe cases of COVID-19 exhibited transient hypercoagulability, reverted by the end of the first month. However, severe COVID-19 cases sustain hypofibrinolysis throughout the course of the disease, which is associated with elevated activity of fibrinolysis inhibitors. Persistent hypofibrinolysis could contribute to long COVID-19 manifestations.

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Resumen El nuevo síndrome respiratorio agudo severo por coronavirus tipo 2 (SARS-CoV-2) que causa la enfermedad por COVID-19, se detectó por primera vez en diciembre de 2019. En donde se ha visto que existe un estado protrombótico con afección al sistema nervioso central, con afectación a vasos de gran calibre como la arteria cerebral media, se debe a mecanismos inducidos por la propia infección, estado de hipercoagulabilidad y daño endotelial. Las manifestaciones neurológicas en el COVID-19 se encuentran en el 36% de los pacientes. Descripción del caso: Se trata de un paciente del sexo masculino, de 36 años de edad, con fiebre, tos y malestar general, a quien se le realizó una prueba COVID que resultó positiva, con empeoramiento del cuadro al que se agregó fotofobia, hemiparesia derecha y desviación de la comisura labial hacia la izquierda, por lo que fue llevado a un facultativo 8 horas después del inicio del cuadro clínico. Ahí se realizó una tomografía de cráneo simple que evidenció infarto extenso de la arteria cerebral media izquierda, con edema cerebral maligno, el cual se derivó a manejo quirúrgico de urgencia donde se le realizó una craniectomía descompresiva izquierda extensa. Después de esto, se mantuvo con asistencia respiratoria por intubación mecánica y medidas antiedema cerebral, y se logró que hubiera progresión ventilatoria; sin embargo, se le realizó traqueostomía y gastrostomía por presentar malos predictores de extubación. Se mantuvo en observación posquirúrgica y quedó con hemiparesia 3/5 derecha, sin algún otro déficit, por lo que se dio egreso a domicilio. Discusión: El caso presentado fue manejado con craniectomía descompresiva extensa, y se obtuvo mejoría en la supervivencia y pronóstico funcional, al igual que lo reportado en la literatura médica, en donde se recomienda que dicho manejo se realice de forma temprana. Conclusiones: El presente informe nos revela que aquellos pacientes hombres jóvenes en la cuarta y quinta década de la vida, con COVID-19 e infarto de arteria cerebral media, se presentan sin comorbilidades al darse tratamiento temprano con hemicraniectomía descompresiva, el cual mejora su pronóstico de vida, concordando con los casos presentados en la literatura médica.

Abstract The new severe acute respiratory syndrome due to coronavirus type 2 (SARS-CoV-2), which causes COVID-19 disease, was detected for the first time in December 2019. Where it has been seen that there is a prothrombotic state with involvement of the Central Nervous, with involvement of large vessels such as the middle cerebral artery, is due to mechanisms induced by the infection itself, hypercoagulable state and endothelial damage. Neurological manifestations in COVID-19 are found in 36% of patients. Case description: This is a 36-year-old male patient with fever, cough and general malaise. A COVID test was performed, which came out positive. His condition was getting worse adding photophobia, right hemiparesis and deviation of the corner of the mouth to the left, which is why he went to the doctor, arriving 8 hours after the onset of the clinical picture, where a simple skull tomography was performed, showing extensive infarction of the left middle cerebral artery with malignant cerebral edema. He was transferred to emergency surgical management where a left decompressive craniectomy was performed. After this, mechanical respiratory assistance with intubation and anti-cerebral edema measures were maintained, achieving ventilatory progression; however, a tracheostomy and gastrostomy were performed due to poor predictors of extubation. He was kept under post-surgical observation, leaving him with 3/5 right hemiparesis, without any other deficit, therefore, he was discharged home. Discussion: The case presented was managed with decompressive craniectomy, resulting in an improvement in survival, as reported in the literature where it is recommended that such management should be performed early. Conclusions: This report reveals that patients with COVID-19 present in young men in the fourth and fifth decade of life, without comorbidities, that recieved early treatment with decompressive hemicraniectomy, improved their life prognosis, consistent with the cases presented in the literature.

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Exacerbated inflammation and coagulation are a hallmark of COVID-19 severity. Extracellular vesicles (EVs) are intercellular transmitters involved in inflammatory conditions, which are capable of triggering prothrombotic mechanisms. Since the release of EVs is potentially associated with COVID-19-induced coagulopathy, the aim of this study was to evaluate changes in inflammation- and hypercoagulability-related EVs during the first month after symptom onset and to determine whether they are associated with disease severity. Blood samples of patients with mild or severe forms of the disease were collected on three occasions: in the second, third and fourth weeks after symptom onset for the quantification by flow cytometry of CD41A (platelet glycoprotein IIb/IIIa), CD162 (PSGL-1), CD31 (PECAM-1) and CD142 cells (tissue factor). Analysis of variance (ANOVA) with repeated measures, Kruskal-Wallis and correlation tests were used. Eighty-five patients were enrolled, 71% of whom had mild disease. Seventeen uninfected individuals served as controls. Compared to controls, both mild and severe COVID-19 were associated with higher EV-CD31+, EV-CD41+ and EV-CD142+ levels. All EV levels were higher in severe than in mild COVID-19 only after the third week from symptom onset, as opposed to C-reactive protein and D-dimer levels, which were higher in severe than in mild COVID-19 earlier during disease progression. EV levels were also associated with C-reactive protein and D-dimer levels only after the third week of symptoms. In conclusion, EVs expressing CD41A, CD31, TF, and CD162 appear as late markers of COVID-19 severity. This finding may contribute to the understanding of the pathogenesis of acute and possibly long COVID-19.

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ABSTRACT Exacerbated inflammation and coagulation are a hallmark of COVID-19 severity. Extracellular vesicles (EVs) are intercellular transmitters involved in inflammatory conditions, which are capable of triggering prothrombotic mechanisms. Since the release of EVs is potentially associated with COVID-19-induced coagulopathy, the aim of this study was to evaluate changes in inflammation- and hypercoagulability-related EVs during the first month after symptom onset and to determine whether they are associated with disease severity. Blood samples of patients with mild or severe forms of the disease were collected on three occasions: in the second, third and fourth weeks after symptom onset for the quantification by flow cytometry of CD41A (platelet glycoprotein IIb/IIIa), CD162 (PSGL-1), CD31 (PECAM-1) and CD142 cells (tissue factor). Analysis of variance (ANOVA) with repeated measures, Kruskal-Wallis and correlation tests were used. Eighty-five patients were enrolled, 71% of whom had mild disease. Seventeen uninfected individuals served as controls. Compared to controls, both mild and severe COVID-19 were associated with higher EV-CD31+, EV-CD41+ and EV-CD142+ levels. All EV levels were higher in severe than in mild COVID-19 only after the third week from symptom onset, as opposed to C-reactive protein and D-dimer levels, which were higher in severe than in mild COVID-19 earlier during disease progression. EV levels were also associated with C-reactive protein and D-dimer levels only after the third week of symptoms. In conclusion, EVs expressing CD41A, CD31, TF, and CD162 appear as late markers of COVID-19 severity. This finding may contribute to the understanding of the pathogenesis of acute and possibly long COVID-19.

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Endothelial dysfunction is a key phenomenon in COVID-19, induced by direct viral endothelial infection and secondary inflammation, mainly affecting the microvascular circulation. However, few studies described the subcellular aspects of the lung microvasculature and the associated thrombotic phenomena, which are widely present in severe COVID-19 cases. To that end, in this transversal observational study we performed transmission and scanning electron microscopy in nine lung samples of patients who died due to COVID-19, obtained via minimally invasive autopsies in Sao Paulo, Brazil, in 2020. All patients died due to acute respiratory failure and had microvascular thrombosis at histology. Electron microscopy revealed areas of endothelial damage with basal lamina disruption and virus infection in endothelial cells. In the capillary lumens, the ultrastructure of the thrombi is depicted, with red blood cells stacking, dysmorphism and hemolysis, fibrin meshworks, and extracellular traps. Our description illustrates the complex pathophysiology of microvascular thrombosis at the cellular level, which leads to some of the peculiar characteristics of severe COVID-19.NEW & NOTEWORTHY In this study, electron microscopy was used to explain the pathophysiology of respiratory failure in severe COVID-19. Before the advent of vaccination, as the virus entered the respiratory system, it rapidly progressed to the alveolar capillary network and, before causing exudative alveolar edema, it caused mainly thrombosis of the pulmonary microcirculation with preserved lung compliance explaining "happy hypoxia." Timing of anticoagulation is of pivotal importance in this disease.

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Background: Autopsy requests have been trending downward for a variety of factors. There are differences between pre- and postmortem diagnoses. Autopsies remain a tool for education, public health research, quality control, and closure for families. Objective: We report two cases that illustrate the utility of autopsy for uncovering contributing factors in the death of these patients and highlight their ongoing importance. Design: Clinical and autopsy investigation of two individuals and illustration of the importance of autopsy findings which, had they been diagnosed premortem, could have changed the outcome. Cases were evaluated using the Goldman criteria for discrepancies between premortem clinical diagnoses and postmortem autopsy findings. Results: In the first case, the patient had been previously admitted due to a non-ST elevation myocardial infarction months before the fatal event. The autopsy showed an undiagnosed clear cell carcinoma of the ovary. She expired due to a massive myocardial infarction secondary to neoplasm induced hypercoagulable state. The degree of pre-mortem/postmortem diagnostic discrepancy makes this a Goldman Class I error.In the second case, the patient presented to the emergency department with symptoms of Guillain-Barré Syndrome (GBS), for which he was treated. Abdominal masses were discovered; however, the patient decompensated before workup was completed. A high-grade B-cell lymphoma was confirmed but would not have altered the outcome, making this a Goldman class II error. Conclusions: The autopsy remains a relevant and necessary tool for physicians and society. It assists in the establishment of diagnoses, measurement of treatment quality, the providence of public health metrics, and closure to the survivors.

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Concerns for the long-term effects of COVID-19 infection have grown due to frequently reported persisting symptoms that can affect multiple systems for longer than 4 weeks after initial infection, a condition known as long-COVID-19 or post-acute COVID-19 syndrome (PACS). Even nonhospitalized survivors have an elevated risk for the development of thromboinflammatory-associated events, such as ischemic stroke and heart failure, pulmonary embolism and deep vein thrombosis. Recent findings point to the persistence of many mechanisms of hypercoagulability identified to be associated with disease severity and mortality in the acute phase of the disease, such as sustained inflammation and endotheliopathy, accompanied by abnormal fibrin generation and impaired fibrinolysis. Platelets seem to be central to the sustained hypercoagulable state, displaying hyperreactivity to stimuli and increased adhesive capacity. Platelets also contribute to elevated levels of thromboinflammatory mediators and pro-coagulant extracellular vesicles in individuals with ongoing PACS. Despite new advances in the understanding of mechanisms sustaining thromboinflammation in PACS, little is known about what triggers this persistence. In this graphical review, we provide a schematic representation of the known mechanisms and consequences of persisting thromboinflammation in COVID-19 survivors and summarize the hypothesized triggers maintaining this prothrombotic state.

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ABSTRACT Background Autopsy requests have been trending downward for a variety of factors. There are differences between pre- and postmortem diagnoses. Autopsies remain a tool for education, public health research, quality control, and closure for families. Objective We report two cases that illustrate the utility of autopsy for uncovering contributing factors in the death of these patients and highlight their ongoing importance. Design Clinical and autopsy investigation of two individuals and illustration of the importance of autopsy findings which, had they been diagnosed premortem, could have changed the outcome. Cases were evaluated using the Goldman criteria for discrepancies between premortem clinical diagnoses and postmortem autopsy findings. Results In the first case, the patient had been previously admitted due to a non-ST elevation myocardial infarction months before the fatal event. The autopsy showed an undiagnosed clear cell carcinoma of the ovary. She expired due to a massive myocardial infarction secondary to neoplasm induced hypercoagulable state. The degree of pre-mortem/postmortem diagnostic discrepancy makes this a Goldman Class I error. In the second case, the patient presented to the emergency department with symptoms of Guillain-Barré Syndrome (GBS), for which he was treated. Abdominal masses were discovered; however, the patient decompensated before workup was completed. A high-grade B-cell lymphoma was confirmed but would not have altered the outcome, making this a Goldman class II error. Conclusions The autopsy remains a relevant and necessary tool for physicians and society. It assists in the establishment of diagnoses, measurement of treatment quality, the providence of public health metrics, and closure to the survivors.

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Background: Thermography is a noninvasive, non-contact, painless, and non-ionizing imaging technique that records cutaneous thermal patterns generated by infrared emission of the surface. The surface heat is closely related to dermal microcirculation. Thromboembolism is responsible for important changes in the thermal pattern of the body surface due to physical obstruction of blood flow, being the main complication in immune-mediated hemolytic anemia. The aim of this paper is to report a dog with thrombus in his left forelimb secondary to idiopathic hemolytic anemia, whose diagnostic screening was performed through infrared thermography. Case: A 9-year-old mixed breed bitch was referred to a veterinary hospital with a history of emesis, diarrhea and dark-colored urine for 2 days. The complete blood count showed hypochromic macrocytic anemia (hematocrit [HTC] 28%, reference: 37 to 55%) with the presence of nucleated erythrocyte (14/100 leukocytes, reference: 0 to 5/100 leukocytes), polychromasia and spherocytes. Leukocytosis (28,300 mm³, reference: 6,000 to 17,000 mm³) by neutrophilia with left deviation and toxic granulations was also present, in addition to hemoglobinuria at urine exam. Therefore, treatment for immune-mediated hemolytic anemia (IMHA) was instituted. After 2 days, the animal returned with acute functional impairment of the left forelimb. Physical examination revealed that the limb was cold, without pulse, proprioception, reflexes, and deep pain. New blood analyses revealed decreased hematocrit (HTC 17%, reference: 37 to 55%), and increased total leukocyte number (57,000 mm3, reference: 6,000 to 17,000 mm³). Infrared thermography revealed an important temperature difference between the limbs, with the affected limb temperature considerably lower (31.3ºC) when compared to the contralateral limb (35.0ºC). Thermography showed the site of the thrombus in the medial portion of the limb (cephalic vein), where the catheter had been placed for fluid therapy. Due to the severity of the condition, the bitch was submitted to amputation surgery, which occurred without complications. The patient had a good response to treatment, with decreased signs of hemolysis and hypercoagulability. The medications were slowly withdrawn, and the clinical discharge occurred after 4 weeks. Discussion: In humans, thermography has been widely used in the assessment of thrombotic diseases, contributing to diagnosis, localization, and prognosis. In veterinary medicine, however, the use of this tool in the diagnosis of thromboembolism is still rare. The difference of 3.7°C between the affected and contralateral limb was objectively verified using thermography. A minimum difference of 2.4°C between limbs has high sensitivity and specificity for diagnosing thromboembolism and occurs due to the reduction in local blood flow. In the present case this tool was essential for the anatomical location of the thrombus, which was in the middle third of the forearm, and allowed an adequate surgical planning. It is known that the main complication of IMHA is thromboembolism. Its predisposing factors include venous stasis, endothelial damage, and hypercoagulability, being exacerbated by cage confinement, decubitus and presence of a peripheral venous catheter. The reported case corroborates at least one of these factors since it had a peripheral venous catheter in the left forelimb, which later showed absence of pulse, spinal reflexes, pain and proprioception. The thermography showed to be an objective, rapid and non-invasive tool to diagnose and precisely locate the thrombus, which allowed for adequate treatment and surgical planning for the case. To the best of our knowledge, this is the first report about use of thermography to diagnose thromboembolism secondary to immune-mediated hemolytic anemia in a dog.

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The SARS-CoV-2 virus was first identified in December 2019, the infection was named COVID-19. The initial symptoms and evolution of the disease have been described over the past year. The virus has been shown to increase the risk of thromboembolic events due to the hypercoagulable state triggered by systemic endothelial inflammation. We present the case of a patient with a history of rheumatoid arthritis under prolonged treatment with tofacitinib, who presented COVID-19 and subsequently developed a hypercoagulable state of approximately 6 months' duration. The possible association between viral infection and the use of tofacitinib is debated.

El virus SARS-CoV-2 se identificó por primera vez en diciembre de 2019; la infección se denominó COVID-19. Los síntomas iniciales y la evolución de la enfermedad se han descrito durante el último anno. Se ha demostrado que el virus aumenta el riesgo de eventos trom-boembólicos debido al estado de hipercoagulabilidad desencadenado por la inflamación endotelial sistêmica. Se presenta el caso de un paciente con antecedente de artritis reuma-toide en tratamiento prolongado con tofacitinib, que presentó COVID-19 y posteriormente desarrolló un estado de hipercoagulabilidad de aproximadamente seis meses de duración. Se debate la posible asociación entre la infección viral y el uso de tofacitinib.

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Hemolytic diseases such as Sickle Cell Disease (SCD) are characterized by a natural propensity for both arterial and venous thrombosis. The ability of heme to induce tissue factor (TF) activation has been shown both in animal models of SCD, and in human endothelial cells and monocytes. Moreover, it was recently demonstrated that heme can induce coagulation activation in the whole blood of healthy volunteers in a TF-dependent fashion. Herein, we aim to further explore the cellular mechanisms by which heme induces TF-coagulation activation, using human mononuclear cells, which have been shown to be relevant to in vivo hemostasis. TF mRNA expression was evaluated by qPCR and TF procoagulant activity was evaluated using a 2-stage assay based on the generation of activated factor X (FXa). Heme was capable of inducing both TF expression and activation in a TLR4-dependent pathway. This activity was further amplified after TNF-α-priming. Our results provide additional details on the mechanisms by which heme is involved in the pathogenesis of hypercoagulability in hemolytic diseases.

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Abstract The hypercoagulable state continues after the Coronavirus 2019 (Covid 19) infection and prophylactic anticoagulants are recommended in this period. However, arterial and venous thromboembolic events can be observed during the convalescence period after the Covid 19. Here, we present the case of acute lower extremity arterial and venous thromboembolism developed in the post-Covid 19 period in a 77-years-old patient, under therapeutic doses of anticoagulant therapy (enoxparin 1mg/kg of weight every 12 hours). The patient, who had no previous history of arterial or venous thrombosis, was taken to emergency surgery with the diagnosis of ALI (acute limb ischemia) due to acute arterial thrombosis. An arterial thrombectomy was performed with the help of a 4F Fogarty catheter inserted from the left femoral artery under local anesthesia. All distal pulses of the patient were palpable in the postoperative period. After the platelet count became >100,000 mm3, 100 mg of acetylsalicylic acid daily was added to the therapeutic dose of enoxaparin sodium treatment. The patient was discharged, uneventfully, except for a minimal diameter increase secondary to deep venous thrombosis (DVT) on the fifth postoperative day, with a combination of enoxaparin and acetylsalicylic acid treatment. Endothelial injury, chronic immuno-thrombogenicity, and increased platelet aggregation in the post-Covid 19 recovery period can cause major thrombotic events, even weeks after the recovery. Anticoagulant therapy is recommended for thromboprophylaxis when the following statuses exist: ≥65 years, critical illness, cancer, prior VTE, thrombophilia, severe immobility, and elevated D- dimer. Combination treatment with long-term antiaggregant therapy may be prudent in thromboembolic events developed under anticoagulant therapy.

Resumen El estado de hipercoagulabilidad continúa después de la infección por Coronavirus 2019 (Covid-19) y la anticoagulación profiláctica se recomienda durante este período. Sin embargo, eventos tromboembólicos arteriales y venosos se pueden observar durante el período de convalecencia posterior al Covid-19. Se presenta el caso de trombosis venosa profunda (TVP) y arterial agudas de una extremidad inferior en una paciente de 77 años, bajo terapia anticoagulante (enoxparin 1mg/kg de peso, cada 12 horas), en el período post- Covid 19. La paciente, sin historia previa de trombosis arterial ni venosa, fue llevada a cirugía de emergencia con el diagnóstico de isquemia aguda de extremidades por trombosis arterial aguda. Se le realizó trombectomía arterial con la ayuda de un catéter Fogarty 4F insertado desde la arteria femoral izquierda bajo anestesia local. Todos los pulsos distales del paciente fueron palpables en el periodo postoperatorio. Después de que las plaquetas llegaron a ser mayores a100.000 mm3, 100 mg de ácido acetilsalicílico diarios se añadieron a la dosis terapéutica del tratamiento con enoxaparina sódica. La paciente fue dada de alta sin incidencias, excepto por un mínimo aumento de diámetro secundario a la TVP, al quinto día postoperatorio con la combinación de enoxaparina y ácido acetilsalicílico. La lesión endotelial, la inmunotrombogenicidad crónica y la agregación plaquetaria aumentada en el período de recuperación posterior a Covid-19 pueden causar eventos trombóticos importantes incluso semanas después de la recuperación. La combinación con terapia antiagregante a largo plazo puede ser prudente en los casos de eventos tromboembólicos desarrollados en pacientes con terapia anticoagulante.

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There is increasing evidence that COVID-19 can be associated with ischemic stroke (COVID-stroke). The frequency and pathogenesis of COVID-stroke, however, remains largely unknown. This narrative review aimed at summarizing and discussing current knowledge about frequency and pathogenesis of COVID-stroke in 455 patients collected from the literature. COVID-stroke occurs in all age groups and predominantly in males. The anterior circulation is more frequently affected than the posterior circulation. COVID-stroke is most frequently embolic. The severity of COVID-stroke ranges from NIHSS 3 to 32. Cardiovascular risk factors are highly prevalent in patients with COVID-stroke. COVID-stroke occurs simultaneously with the onset of pulmonary manifestations or up to 40 days later. Clinical manifestations of COVID-19 are most frequently mild or even absent. The majority of patients with COVID-stroke achieve complete or partial recovery, but in one-quarter of patients, the outcome is fatal. In conclusion, the frequency of ischemic stroke has not increased since the outbreak of the SARS-CoV-2 pandemic. COVID-stroke predominantly affects males and the anterior circulation. COVID-stroke is multifactorial but predominantly embolic and more frequently attributable to cardiovascular risk factors than to coagulopathy.

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Resumen: La frecuencia de eventos tromboembólicos de pacientes con enfermedad por coronavirus es alta, sin embargo aún se desconoce cuál es la manera adecuada de identificar a las personas con mayor riesgo de complicaciones trombóticas y definir quiénes pueden beneficiarse de un tratamiento más agresivo, más allá de la tromboprofilaxis estándar. Una gran proporción de pacientes en estado crítico con coronavirus tienen perfil de tromboelastografía hipercoagulable con daño relacionado a fibrinógeno y a la función plaquetaria, la mayoría de pacientes tiene una máxima amplitud elevada en la tromboelastografía. Se hizo una revisión de tromboelastogramas de 11 pacientes en estado crítico por SARS-CoV-2 para caracterizar su estado de coagulación. Se encontró 36.36% de hipercoagulabilidad en la tromboelastografía principalmente con citrato nativo a pesar del tratamiento con heparina de bajo peso molecular a dosis terapéutica. El perfil predominante hipercoagulable no se asoció a la función plaquetaria, ya que la MA (máxima amplitud) se mantuvo dentro de los límites normales.

Abstract: The frequency of thromboembolic events in patients with coronavirus disease is high, however it is still unknown what is the appropriate way to identify people at higher risk of thrombotic complications and define who can benefit from a more aggressive treatment, beyond the standard thromboprophylaxis. A large proportion of critically ill patients with coronavirus have a hypercoagulable thromboelastography profile with damage related to fibrinogen and platelet function; most patients have a high maximum amplitude on thromboelastography. A review of thromboelastograms of 11 critically ill patients due to SARS-CoV-2 was made to characterize their coagulation status. A 36.36% hypercoagulability was found in thromboelastography, mainly with native citrate, despite treatment with low molecular weight heparin at therapeutic doses. The predominant hypercoagulable profile was not associated with platelet function since the MA (maximum amplitude) remained within normal limits.

Resumo: A frequência de eventos tromboembólicos em pacientes com doença por coronavírus é alta, no entanto, ainda não se sabe qual é a forma adequada de identificar as pessoas com maior risco de complicações trombóticas e definir quem pode se beneficiar de um tratamento mais agressivo, além da tromboprofilaxia padrão. Uma grande proporção de pacientes críticos com coronavírus apresenta um perfil de tromboelastografia hipercoagulável com danos relacionados ao fibrinogênio e função plaquetária, a maioria dos pacientes apresentam uma amplitude máxima elevada na tromboelastografia. Foi feita uma revisão de tromboelastogramas de 11 pacientes en estado crítico devido a SARS-CoV-2 para caracterizar seu estado de coagulação. Encontrou-se hipercoagulabilidade de 36.36% na tromboelastografia, principalmente com citrato nativo, apesar do tratamento com heparina de baixo peso molecular em dose terapêutica. O perfil predominantemente hipercoagulável não foi associado à função plaquetária, uma vez que a AM (amplitude máxima) permaneceu dentro dos limites da normalidade.

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ABSTRACT There is increasing evidence that COVID-19 can be associated with ischemic stroke (COVID-stroke). The frequency and pathogenesis of COVID-stroke, however, remains largely unknown. This narrative review aimed at summarizing and discussing current knowledge about frequency and pathogenesis of COVID-stroke in 455 patients collected from the literature. COVID-stroke occurs in all age groups and predominantly in males. The anterior circulation is more frequently affected than the posterior circulation. COVID-stroke is most frequently embolic. The severity of COVID-stroke ranges from NIHSS 3 to 32. Cardiovascular risk factors are highly prevalent in patients with COVID-stroke. COVID-stroke occurs simultaneously with the onset of pulmonary manifestations or up to 40 days later. Clinical manifestations of COVID-19 are most frequently mild or even absent. The majority of patients with COVID-stroke achieve complete or partial recovery, but in one-quarter of patients, the outcome is fatal. In conclusion, the frequency of ischemic stroke has not increased since the outbreak of the SARS-CoV-2 pandemic. COVID-stroke predominantly affects males and the anterior circulation. COVID-stroke is multifactorial but predominantly embolic and more frequently attributable to cardiovascular risk factors than to coagulopathy.

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RESUMEN: Presentamos el caso clínico de un varón de 58 años de edad, con trombosis por déficit de Proteína C y S, tras descartar proceso secundario, inmunológico y oncológico.

ABSTRACT: We present the clinical case of a 58-year-old man with protein C and S deficiency thrombosis, after ruling out secondary, immunological and oncological processes.

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Introducción: En los últimos años se ha comprobado que el riesgo de trombosis en pacientes con enfermedades oncohematológicas es elevado. Presentación del caso: Paciente masculino de 51 años de edad, con diagnóstico de leucemia promielocítica, recibió tratamiento de inducción con trióxido de arsénico y ya alcanzada la remisión morfológica de la leucemia, y sin antecedentes personales ni familiares de eventos trombóticos, presentó una trombosis venosa profunda del miembro inferior izquierdo, se trató con heparina de bajo peso molecular y warfarina. Conclusiones: El paciente evolutivamente tuvo una evolución favorable del evento trombótico y se alcanzó la remisión completa hematológica, citogenética y molecular con una adecuada calidad de vida que permitió su reinserción a su vida personal, familiar y social(AU)

Introduction: In recent years it has been proven that the risk of thrombosis in patients with oncohematological diseases has increased. Case presentation: A 51-year-old male patient, diagnosed with Promyelocytic Leukemia, received induction treatment with arsenic trioxide and the morphological remission of the leukemia had already been achieved and with no personal or family history of thrombotic events, presented a deep vein thrombosis of the left lower limb. He was treated with low molecular weight heparin and warfarin. Conclusions: The patient progressively had a favorable evolution of the thrombotic event and complete hematological, cytogenetic and molecular remission was achieved with an adequate quality of life that allowed his reinsertion into his personal, family and social life(AU)

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COVID-19 is a contagious infectious disease, which quickly spreads worldwide, whose clinical presentation includes from mild flu-like symptoms to pneumonia and severe acute respiratory syndrome. The severe presentation of the disease can affect different organs and systems. Coagulopathy has been associated with a worse clinical outcome, with manifestations such as pulmonary embolism and systemic arterial thrombosis. Thromboelastometry has been used to identify hypercoagulability in early stages of disease. We report the case of a 59-year-old woman with COVID-19 infection complicated by pulmonary embolism and acute arterial thrombosis associated with critical lower limb ischemia requiring amputation. This report showed a case of thrombotic complication in patient with infection caused by novel coronavirus 2019 whose thromboelastometry allowed the early identification of hypercoagulability pattern. This is a single case report and the use of thromboelastometry should be further evaluated in large prospective cohort studies.

RESUMO

Resumen La vasculopatía livedoide (VL), es una enfermedad vascular oclusiva que afecta la microvasculatura, se caracteriza por ser recurrente y no inflamatoria. Su incidencia es de 1/100.000 casos por habitantes, afectando en su mayoría a mujeres de edad media. Su patogenia se desconoce, pero se destaca el componente trombótico de la misma, causado por un estado de hipercoagulabilidad, que conduce a la oclusión vascular, debiendo distinguirse una forma primaria y una secundaria.Clínicamente se observan úlceras dolorosas a nivel maleolar que evolucionan progresivamente a una cicatrización atrófica, blanquecina nacarada y estrellada característica.Presentamos un caso clínico en un varón con múltiples comorbilidades y difícil tratamiento, el cual requirió un trabajo multidisciplinario.

Abstract Livedoid vascular disease (VL), is an occlusive vascular disease that affects the microvasculature, is characterized by being recurrent and non-inflammatory. Its incidence is 1 / 100,000 cases per inhabitant, affecting mostly middle-aged women. Its pathogenesis is unknown, but its thrombotic component stands out, caused by a state of hypercoagulability, which leads to vascular occlusion, and a primary and secondary form must be distinguished. Clinically, painful ulcers are observed at the malleolar level, progressing progressively to characteristic atrophic, pearly whitish and starry healing. We present a clinical case in a male with multiple comorbidities and difficult management, which required multidisciplinary work.