Intracerebral haemorrhage and COVID-19: Clinical characteristics from a case series

Abstract

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Intracranial Hemorrhage in Hospitalized SARS-CoV-2 Patients: A Case Series

“…D-dimer and fibrin split products) and other non-specific indicators such as ferritin, C-reactive protein, erythrocyte sedimentation rate, and lactate dehydrogenase which may represent the widespread endothelial damage thought to be associated with COVID-19. ( 9 , 10 , 12 , 13 ) However, therapeutic anticoagulation comes with an increased risk of bleeding. Evidence of the overall effect of therapeutic anticoagulation in critically ill COVID-19 patients without confirmed thrombosis is lacking.…”

Risk factors for intracerebral hemorrhage in patients with COVID-19

“…These hypoxic patients might have hypoxia induced blood brain barrier disruption (similar what occurs in high altitude cerebral edema) leaving them more susceptible to ICH [ 26 ]. Alternatively, the downstream effects of the hypoxic, inflammatory milieu might contribute to endothelial dysfunction and cerebral injury [ 27 ]. Endothelial damage has been shown to occur in SARS-CoV-2 [ 28 , 29 ] and microscopic disruption of the endothelium of cerebral veins could lead to microbleeds and eventual ICH [ 27 ].…”

“…Alternatively, the downstream effects of the hypoxic, inflammatory milieu might contribute to endothelial dysfunction and cerebral injury [ 27 ]. Endothelial damage has been shown to occur in SARS-CoV-2 [ 28 , 29 ] and microscopic disruption of the endothelium of cerebral veins could lead to microbleeds and eventual ICH [ 27 ]. Another proposed hypothesis is the microvascular thrombosis suggested to result in hypoxemic respiratory failure in some patients with COVID-19 might also result in direct neural injury and/or the microbleeds observed in patients with COVID-19 [ 30 – 32 ] Microbleeds could portend further risks for cerebral hemorrhage, particularly in the setting of anticoagulation use [ 11 , 32 , 33 ].…”

The Neurological Complexities and Prognosis of COVID-19

“…The pathogenesis of intracerebral hemorrhage in COVID-19 patients is best understood by the binding of SARS-CoV-2 to ACE2 receptors on the endothelial cells. This binding results in the destruction of ACE2 receptors fundamentally compromising the integrity of the blood brain barrier and allowing the virus to enter the CNS [7,30]. Plus, decreased expression of ACE2 receptors can negatively impact the renin-angiotensin system (RAS) complicating the regulation of the CNS and PNS system affecting the regulation of blood pressure, potentially resulting in intracerebral hemorrhage [7,30].…”

“…There were no underlying conditions such as hypertension or anticoagulation that predisposed him to an intracerebral hemorrhage [15]. In patients infected with COVID-19, reports of large vessel occlusion and infarcts, venous thromboembolism, raised inflammatory markers, and severe systemic inflammations with organ failure including the brain, are occurring at an alarming rate [31]. Physicians have to base decisions on administration anticoagulation with the risk of thrombosis versus the risk of hemorrhage [31].…”