Encephalopathy as the Only Manifestation in Simultaneous Arterial Infarct and Cerebral Venous Sinus Thrombosis in Recent COVID-19 Infection.

BACKGROUND Emerging cases of SARS-CoV-2 infection associated with cerebral thromboembolism episodes manifesting as arterial strokes or cerebral venous thrombosis have been reported. However, the co-occurrence of arterial strokes and cerebral venous thrombosis is rare. CASE REPORT We report the case of a previously healthy young patient with recent SARS-CoV-2 infection, who presented with encephalopathy. His computed tomography venography and magnetic resonance imaging of the brain showed thrombosis of the vein of Galen and straight sinus, and arterial infarcts in both hemispheres. His inflammatory markers, D-dimer levels, and coagulation profile were normal. He was started on anticoagulation and recovered well. CONCLUSIONS Concurrent arterial and venous thrombosis can happen rarely in patients with SARS-CoV-2 infection, including patients who have recently recovered from COVID-19. Cerebral thromboembolism associated with SARS-CoV-2 can present with a variety of subtle clinical manifestations, including encephalopathy without focal neurological deficits. Inflammatory markers, D-dimer levels, and coagulation profiles can be normal, especially in patients with mild infection or who have recovered from the infection. Therefore, it is important to be vigilant and recognize this clinical entity so that the diagnosis can be made and treatment can be started promptly. However, larger and prospective studies are needed to determine the clinical outcomes, therapeutic benefits, and complications of concurrent arterial stroke and cerebral venous thrombosis associated with SARS-CoV-2 infection.

Post-COVID-19 superior mesenteric artery and jejunal branches thromboembolism.

The World Health Organization has declared the novel coronavirus disease 2019 (COVID-19) a global public health emergency. Despite the predominating respiratory symptoms occurring in COVID-19, thrombosis can occur in some patients, with morbidity and mortality increase due to the respiratory worsening. This article reports the case of a 62-year-old man with a flu-like illness that was diagnosed as COVID-19 by RT-PCR of SARS-CoV-2. After three weeks, he subsequently developed abdominal pain in addition to bloating, nausea, and vomiting. He underwent exploratory laparotomy after imaging tests suggested mesenteric ischemia. Intestinal ischemia was evident, due to the absence of flow in the superior mesenteric artery and jejunal branches. Embolectomy and enterectomy were performed and they resulted in a favorable outcome, with clinical improvement. This case adds data to the limited literature on extrapulmonary complications of COVID-19, notably those related to thromboembolic events.

La Organización Mundial de la Salud ha declarado la enfermedad del nuevo coronavirus 2019 (COVID-19) una emergencia de salud pública mundial. A pesar de los síntomas respiratorios predominantes en COVID-19, la trombosis puede ocurrir en algunos pacientes, con un aumento de la morbimortalidad debido al empeoramiento respiratorio. Presentamos el caso de un hombre de 62 años con enfermedad similar a la gripe que fue diagnosticada como COVID-19 por RT-PCR de SARS-CoV-2. Después de tres semanas, desarrolló dolor abdominal además de hinchazón, náuseas y vómitos. Fue sometido a laparotomía exploradora luego de que las pruebas de imagen sugirieran isquemia mesentérica. Se evidenció isquemia intestinal por ausencia de flujo en la arteria mesentérica superior y ramas yeyunales. Se realizó embolectomía y enterectomía con evolución favorable, con mejoría clínica. Este caso añade datos a la limitada literatura sobre las complicaciones extrapulmonares del COVID-19, en particular las relacionadas con eventos tromboembólicos.

Antiphospholipid antibodies and vitamin D deficiency in COVID-19 infection with and without venous or arterial thrombosis: A pilot case-control study.

BACKGROUND: Coronavirus disease-2019 (COVID-19) is associated with thromboembolism. Antiphospholipid antibody (APLa) formation is one of the mechanisms. Vitamin D deficiency has been associated with thrombosis in antiphospholipid antibody syndrome. OBJECTIVE: Measure APLa and vitamin D in hospitalized COVID-19 patients with and without thrombosis to evaluate if thromboembolism is associated with concomitant APLa and vitamin D deficiency. METHODS: Case-control study. Hospitalized COVID-19 patients with a thromboembolic event (ischemic stroke, myocardial infarction, deep venous thrombosis/pulmonary embolism, Cases n = 20). Controls (n = 20): Age, sex-matched without thromboembolic events. Patients with autoimmune disorders, antiphospholipid antibody syndrome, thrombophilia, anticoagulation therapy, prior thromboembolism, chronic kidney disease 3b, 4, end-stage renal disease, and malignancy were excluded. Given the limited current literature on the role of concomitant antiphospholipid antibodies and vitamin D deficiency in causing venous and/or arterial thrombosis in hospitalized COVID-19 patients, we enrolled 20 patients in each arm. Anti-cardiolipin IgG/IgM, beta-2 glycoprotein-1 IgG/IgM, lupus anticoagulant and vitamin D levels were measured in both groups. RESULTS: Cases were 5.7 times more likely to be vitamin D deficient (OR:5.7, 95% CI:1.3-25.6) and 7.4 times more likely to have any one APLa (OR:7.4, 95% CI: 1.6-49.5) while accounting for the effects of sex. Patients with both APLa and vitamin D deficiency had significantly more thrombosis compared to patients who were antibody positive without vitamin D deficiency (100% vs 47.4%; p = 0.01). CONCLUSIONS: Thrombosis in COVID-19 was associated with concomitant APLa and vitamin D deficiency. Future studies in COVID-19 should assess the role of vitamin D in reducing thrombosis.

Management of a COVID-19 Patient during ECMO: Paying Attention to Acquired von Willebrand Syndrome.

Patients with severe COVID-19 often experience complications including coagulopathy and fatal thrombosis. COVID-19 pneumonia sometimes leads to acute respiratory distress syndrome, requiring extracorporeal membrane oxygenation (ECMO), during which thrombosis and bleeding are major causes of death. Anticoagulation such as heparin is essential for COVID-19 patients on ECMO; however, bleeding might be caused by not only heparin, but also acquired von Willebrand syndrome (AVWS). To date, no study has examined ECMO-related bleeding and AVWS in COVID-19 patients.We report a COVID-19 patient who experienced bleeding from AVWS in addition to disseminated intravascular coagulation (DIC) during ECMO. The level of high-molecular weight VWF multimers decreased during ECMO therapy, and these findings promptly improved after discontinuation of ECMO. Plasma levels of VWF antigen were extremely high, probably due to endothelial cell damage caused by COVID-19. On the other hand, plasma levels of ADAMTS13 activity were moderately reduced, to 20-30% of normal. The patient was successfully treated with cryoprecipitate in bleeding during ECMO without a reduction in heparin, which might have induced thromboembolism. Bleeding found in this patient might be caused by AVWS and DIC.Severe COVID-19 patients are in a thrombotic state and need to receive anticoagulant therapy. However, once they receive ECMO therapy, bleeding symptoms could be observed. In such cases, physicians should think of AVWS in addition to the side effect of heparin and DIC.

Cause-specific death in hospitalized individuals infected with SARS-CoV-2: more than just acute respiratory failure or thromboembolic events.

Infection with SARS-CoV-2 is becoming the leading cause of death in most countries during the 2020 pandemic. The objective of this study is to assess the association between COVID-19 and cause-specific death. The design is retrospective cohort study. We included data from inpatients diagnosed with COVID-19 between March 18 and April 21, 2020, who died during their hospital stay. Demographic, clinical and management data were collected. Causes of death were ascertained by review of medical records. The sample included 128 individuals. The median age was 84 (IQR 75-89), 57% were men. In 109 patients, the death was caused by SARS-CoV-2 infection, whereas in 19 (14.8%, 95 CI 10-22%), the infection acted only as a precipitating factor to decompensate other pathologies. This second group of patients was older (88y vs 82, p < 0.001). In age-adjusted analysis, they had a greater likelihood of heart failure (OR 3.61 95% CI 1.15-11.32), dependency in activities of daily living (OR 12.07 95% CI 1.40-103.86), frailty (OR 8.73 95% CI 1.37-55.46). The presence of X-ray infiltrates was uncommon (OR 0.07, 95% CI 0.02-0.25). A higher percentage of patient deaths from causes unrelated to COVID-19 complications occurred during the two first weeks of the pandemic. Fifteen percent of patients with COVID-19 infection died from decompensation of other pathologies and the cause of death was unrelated to COVID-19 severe complications. Most of these patients had more comorbidities and were frail and elderly. These findings can partially explain the excess mortality in older people.