Subarachnoid hemorrhage: management considerations for COVID-19

Abstract

Subarachnoid hemorrhage (SAH) has deleterious outcomes for patients, and during the hospital stay, patients are susceptible to vasospasm and delayed cerebral ischemia. Coronavirus disease 2019 (COVID-19) has been shown to worsen hypertension through angiotensin-converting enzyme 2 (ACE2) activity, therefore, predisposing to aneurysm rupture. The classic renin-angiotensin pathway activation also predisposes to vasospasm and subsequent delayed cerebral ischemia. Matrix metalloproteinase 9 upregulation can lead to an inflammatory surge, which worsens outcomes for patients. SAH patients with COVID-19 are more susceptible to ventilator-associated pneumonia, reversible cerebral vasoconstriction syndrome, and respiratory distress. Emerging treatments are warranted to target key components of the anti-inflammatory cascade. The aim of this review is to explore how the COVID-19 virus and the intensive care unit (ICU) treatment of severe COVID can contribute to SAH.

Feasibility of FDCT Early Brain Parenchymal Blood Volume Maps in Predicting Short-Term Prognosis in Patients With Aneurysmal Subarachnoid Hemorrhage

“…Future studies with a larger patient population and long-term outcomes will be conducted to explore the diagnostic threshold for PBV so as to make more objective and accurate predictions, and guide clinical interventions in a timely manner ( 52 ). During the COVID-19 pandemic, not only was the coronavirus likely to worsen hypertension and make aneurysms more prone to rupture, but intensive care unit (ICU) resources were more strained, leaving patients more vulnerable ( 53 ). PBV may help in the future to early identify SAH patients with severe brain injury and a possible poor prognosis to better allocate medical resources to those most in need.…”

SARS-CoV-2 infection increases risk of intracranial hemorrhage

“…The SARS-CoV-2 virus uses the angiotensin-converting enzyme 2 (ACE2) receptor, which is highly expressed in the epithelial cells of the lung. As the SARS-CoV-2 virus binds to the ACE2 receptor, the activity of the alternative anti-inflammatory RAS pathway resulting from ACE2-angiotensin interaction is diminished and the classical RAS pathway dominates leading to inflammation, vasoconstriction, water retention, and increased ROS, which consequently can increase the risk of aneurysm rupture due to the hypertensive and ischemic effects of COVID-19 ( Panther and Lucke-Wold, 2022 ; Small et al, 2022 ). Moreover, three other mediators, including extracellular matrix metalloproteinase inducer (CD147) ( Chen et al, 2005 ), sialic acid ( Tortorici et al, 2019 ), and transmembrane serine protease 2 ( Matsuyama et al, 2020 ), have been suggested to mediate the cellular entry of the virus.…”

“…The presence of SARS-Cov-2 elements in endothelial cells and the accumulation of inflammatory cells accompanied by endothelial and inflammatory cell death has been reported ( Varga et al, 2020 ). This damage to endothelial cells by increasing the expression of tissue factors can lead to clotting cascade activation resulting in clot formation, which can lead to stroke when lodged in brain vessels, and these clots via partially blocking vessels can cause turbulent flow that can subsequently lead to aneurysm rupture ( Panther and Lucke-Wold, 2022 ; Small et al, 2022 ). It is already known that cytokine storm (hypercytokinemia) resulting in increased systemic inflammation with high levels of IL-6, IL-1β, and TNFα is induced by viral infections, including influenza A and COVID-19 ( Muhammad et al, 2011 ; Qin et al, 2020 ).…”

“…It is already known that cytokine storm (hypercytokinemia) resulting in increased systemic inflammation with high levels of IL-6, IL-1β, and TNFα is induced by viral infections, including influenza A and COVID-19 ( Muhammad et al, 2011 ; Qin et al, 2020 ). The elevated systemic inflammatory status in COVID-19 patients via increasing blood brain barrier permeability can increase MMP-9 and MMP-9 by the dysregulated breakdown of arterial collagen can lead to arterial instability and can consequently result in ICH and aneurysm aSAH ( Panther and Lucke-Wold, 2022 ). All this basic science work clearly provides a mechanistic explanation for SARS-Cov-2 to possibly involve in stroke or stroke-like diseases.…”

Current Landscape of Mesenchymal Stem Cell Therapy in COVID Induced Acute Respiratory Distress Syndrome

“…MSC therapy could perhaps also be useful for the treatment of other COVID-19 induced complications such as subarachnoid haemorrhage (SAH), myocarditis, acute kidney injury, etc. which are brought on by the host's hyper active immune system[45,46]. However, further studies need to be conducted in order to determine the efficacy of MSC therapy on such COVID-19 induced complications.…”