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Hemorrhagic stroke
Original research
Decrease in cortical vein opacification predicts outcome after aneurysmal subarachnoid hemorrhage
  1. William S Dodd1,
  2. Orrin Dayton2,
  3. Brandon Lucke-Wold3,
  4. Christian Reitano2,
  5. Zachary Sorrentino3,
  6. Katharina M Busl3,4
  1. 1 College of Medicine, University of Florida, Gainesville, Florida, USA
  2. 2 Department of Radiology, University of Florida, Gainesville, Florida, USA
  3. 3 Department of Neurosurgery, University of Florida, Gainesville, Florida, USA
  4. 4 Department of Neurology, University of Florida, Gainesville, Florida, USA
  1. Correspondence to Dr Katharina M Busl, Department of Neurology, University of Florida, Gainesville, FL 32611, USA; katharina.busl{at}neurology.ufl.edu

Abstract

Background The pathophysiology of brain injury after aneurysmal subarachnoid hemorrhage (aSAH) remains incompletely understood. Cerebral venous flow patterns may be a marker of hemodynamic disruptions after aneurysm rupture. We hypothesized that a decrease in venous filling after aSAH would predict cerebral ischemia and poor outcome.

Objective To examine the hypotheses that venous filling as measured by the cortical venous opacification score (COVES) would (1) decrease after aSAH and (2) that decreased COVES would be associated with higher rates of hydrocephalus, vasospasm, delayed cerebral iscemia (DCI), and poor functional evaluation at outcome.

Methods In this retrospective observational cohort study of consecutive patients with aSAH admitted to our tertiary care center between 2016 and 2018, we measured the COVES at admission and at subsequent CT angiography (CTA). We collected clinical variables and compared hydrocephalus, vasospasm, DCI, and outcome at discharge in patients with decrease in COVES with patients with stable COVES.

Results A total of 22 patients were included in the analysis. COVES decreased from first CTA to second CTA in 11 (50%) patients, by an average of 1.1 points (P=0.01). Patients whose COVES decreased between admission and follow-up imaging were more likely to develop DCI (58% vs 0%, P=0.03) and have a poor outcome at discharge (100% vs 55%, P=0.03) than patients who had no change in COVES. aSAH severity was not associated with initial COVES, and there was no association between change in COVES and development of hydrocephalus or vasospasm.

Conclusions Development of decreased venous filling on CTA is associated with poor outcome after aSAH. This association suggests that venous hemodynamics may be reflective of, or contribute to, the pathophysiological mechanisms of brain injury after aSAH. Larger prospective studies are necessary to substantiate our findings.

  • Hemorrhage
  • CT Angiography
  • Stroke
  • Vein

Data availability statement

Data are available upon reasonable request.

https://doi.org/10.1136/jnis-2022-019578

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    Data availability statement

    Data are available upon reasonable request.

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    Footnotes

    • Contributors WSD: conceptualization, methodology, data collection, data curation, formal analysis, visualization, writing – original draft, writing – review and editing. OD: conceptualization, methodology, data collection, data curation, writing – review and editing. BL-W: conceptualization, methodology, data collection, data curation, formal analysis, visualization, writing – review and editing. CR: conceptualization, data collection, data curation, writing – review and editing. ZS: conceptualization, data collection, data curation, writing – review and editing. KMB: conceptualization, methodology, data curation, formal analysis, writing – original draft, writing – review and editing, project administration. KMB is the overall guarantor of the study.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.