Venous cerebral thrombosis in COVID-19 patient

Garaci, Francesco; Giuliano, Francesca Di; Picchi, Eliseo; Ros, Valerio Da; Floris, Roberto

doi:10.1016/j.jns.2020.116871

Cited by 63 publications

(61 citation statements)

References 5 publications

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“…Other three studies described the cases of ischemic stroke concomitant with COVID-19: the patient reported by Co and colleagues [25] was a 62-year-old woman with several pre-existing pathologies such as hypertension, diabetes, dyslipidemia and transient ischemic attack; the patient reported by Frisullo and colleagues [33] was a young woman with no concomitant pathologies, while Zhai and colleagues' [62] patient was a 79-year-old-man. Cerebrovascular complications caused by SARS-CoV-2 infection were also reported by Garaci and colleagues [35]. The authors described a 44-year-old woman with negative past medical history, who developed thrombosis of the superior vena cava, pulmonary artery and deep intracerebral venous thrombosis.…”

Section: Effects Of Sars-cov-2 On Cnsmentioning

confidence: 64%

Neurological Complications of COVID-19 and Possible Neuroinvasion Pathways: A Systematic Review

Orrù

Conversano

Malloggi

et al. 2020

IJERPH

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The Coronavirus Disease 2019 (COVID-19) outbreak has shocked the whole world with its unexpected rapid spread. The virus responsible for the disease, the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), enters host cells by means of the envelope spike protein, which binds to angiotensin-converting enzyme 2 receptors. These receptors are highly expressed in heart, lungs, respiratory tract epithelium, endothelial cells and brain. Since an increasing body of significant evidence is highlighting a possible neuroinvasion related to SARS-CoV-2, a state of the art on the neurological complications is needed. To identify suitable publications, our systematic review was carried out by searching relevant studies on PubMed and Scopus databases. We included studies investigating neurologic manifestations of SARS-CoV-2 in patients over 18. According to the analyzed studies, the most frequent disorders affecting central nervous system (CNS) seem to be the following: olfactory and taste disorders, ischemic/hemorrhagic stroke, meningoencephalitis and encephalopathy, including acute necrotizing encephalopathy, a rare type of encephalopathy. As regards the peripheral nervous system (PNS), Guillain-Barré and Miller Fisher syndromes are the most frequent manifestations reported in the literature. Important clinical information on the neurological manifestations of SARS-CoV-2 would help clinicians raise awareness and simultaneously improve the prognosis of critically ill patients.

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Section: Effects Of Sars-cov-2 On Cnsmentioning

confidence: 64%

Neurological Complications of COVID-19 and Possible Neuroinvasion Pathways: A Systematic Review

Orrù

Conversano

Malloggi

et al. 2020

IJERPH

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“…Another pathway for platelet activation in COVID-19 is via the altered ACE1/ACE2 function. Bradykinin is cleaved by ACE1 into metabolites such as vasoactive bradykinin (1)(2)(3)(4)(5)(6)(7)(8) and des-Arg9-bradykinin that are further degraded by ACE2. In the absence of ACE2, des-Arg9-bradykinin accumulation can activate both neutrophils and platelets into an inflammatory phenotype [108].…”

Section: Platelet Dysfunctionmentioning

confidence: 99%

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

2020

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The pathogenesis of Coronavirus disease 2019 (COVID-19) is gradually being comprehended. A high number of thrombotic episodes are reported, along with the mortality benefits of heparin. COVID-19 can be viewed as a prothrombotic disease. We overviewed the available evidence to explore this possibility. We identified various histopathology reports and clinical case series reporting thromboses in COVID-19. Also, multiple coagulation markers support this. COVID-19 can be regarded as a risk factor for thrombosis. Applying the principles of Virchow's triad, we described abnormalities in the vascular endothelium, altered blood flow, and platelet function abnormalities that lead to venous and arterial thromboses in COVID-19. Endothelial dysfunction, activation of the renin-angiotensin-aldosterone system (RAAS) with the release of procoagulant plasminogen activator inhibitor (PAI-1), and hyperimmune response with activated platelets seem to be significant contributors to thrombogenesis in COVID-19. Stratifying risk of COVID-19 thromboses should be based on age, presence of comorbidities, D-dimer, CT scoring, and various blood cell ratios. Isolated heparin therapy may not be sufficient to combat thrombosis in this disease. There is an urgent need to explore newer avenues like activated protein C, PAI-1 antagonists, and tissue plasminogen activators (tPA). These should be augmented with therapies targeting RAAS, antiplatelet drugs, repurposed antiinflammatory, and antirheumatic drugs.

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“…Our case suggests that hypercoagulability and thromboin ammation associated with COVID-19 [5] may cause CVT in the late phase of infection, a few weeks after the onset of mild respiratory symptoms. In the last month, a few cases of COVID-19 associated CVT were reported, mostly with fatal or unreported outcome [6][7][8][9][10]. In our case, CVT occurred simultaneously with an asymptomatic internal iliac vein thrombosis and both venous thromboses were effectively treated with intravenous UFH followed by subcutaneous LMWH.…”

Section: Resultsmentioning

confidence: 66%

Massive cerebral venous thrombosis related to oligosymptomatic COVID-19 infection: a case report

Beretta

Francioni

et al. 2020

Preprint

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Background: The development of thrombotic coagulopathy is frequent in COVID-19 patients, but the timing after infection, cerebral venous system involvement, treatment and outcome are uncertain.Case Presentation: We report a case of massive cerebral venous thrombosis occurring in the late phase of COVID-19 infection. Mild respiratory symptoms, without fever, started three weeks before headache and acute neurological deficits. She had no dyspnea, although she was hypoxic and with typical COVID-19 associated interstitial pneumonia. Brain CT scan showed a left parietal hypodense lesion with associated sulcal subarachnoid haemorrhage. CT angiography showed a massive cerebral vein thrombosis. An asymptomatic concomitant right internal iliac vein thrombosis was found. Both cerebral venous thrombosis and deep venous thrombosis were effectively treated with unfractionated heparin started on the day of admission, then shifted to low molecular weight heparin, with a favorable clinical course. Nasopharyngel swab, repeated twice, tested negative for SARS-CoV-2. Serological tests confirmed SARS-CoV-2 infection. Conclusions: Our case supports active surveillance and prevention of thrombotic complications associated with COVID-19, which may affect both peripheral and cerebral venous system. Early initiation of unfractionated heparin may lead to good neurological outcome.

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Venous cerebral thrombosis in COVID-19 patient

Cited by 63 publications

References 5 publications

Neurological Complications of COVID-19 and Possible Neuroinvasion Pathways: A Systematic Review

Neurological Complications of COVID-19 and Possible Neuroinvasion Pathways: A Systematic Review

Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow’s triad

Massive cerebral venous thrombosis related to oligosymptomatic COVID-19 infection: a case report

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