CEREBRAL VASOSPASM FOLLOWING ARTERIOVENOUS MALFORMATION RUPTURE: A POPULATION-BASED CROSS SECTIONAL STUDY

Author Type(s)

Faculty, Resident/Fellow

Document Type

Abstract

Publication Date

2022

Journal Title

Journal of NeuroInterventional Surgery

Department

Neurology

Second Department

Neurosurgery

Abstract

Introduction/Purpose Limited evidence exists characterizing the incidence, risk factors, and clinical outcomes of arterial vasospasm secondary to cerebral arteriovenous malformation (cAVM) rupture. We utilize a population-based national registry to investigate this largely unexamined clinical entity. Materials and Methods Weighted discharge data from the National Inpatient Sample during the period of 2015 to 2019 were queried to identify adult ruptured cAVM patients and subsequently those developing angiographically-confirmed vasospasm. Complex samples multivariable logistic regression and chi-square automatic interaction detection (CHAID) decision tree analyses were performed to identify significant associations between clinical covariates and the development of vasospasm, and a cAVM vasospasm predictive model (cAVM-VPM) was generated based on the effect sizes of these parameters. Results Among 7,215 cAVM patients identified, 935 developed vasospasm, corresponding to an incidence of 13.0%. 110 of these patients (11.8%) subsequently progressed to delayed cerebral ischemia (DCI). Multivariable adjusted modeling identified baseline clinical covariates [decreasing age (by decade) (aOR 0.87, 95% CI 0.83, 0.92; p < 0.001), female sex (aOR 1.68, 95% CI 1.45, 1.95; p < 0.001), admission Glasgow Coma Scale score < 9 (aOR 1.34, 95% CI 1.01, 1.79; p = 0.045), intraventricular hemorrhage (aOR 1.87, 95% CI 1.17, 2.98; p = 0.009), hypertension (aOR 1.77, 95% CI 1.50, 2.08; p < 0.001), obesity (aOR 0.68, 95% CI 0.55, 0.84; P < 0.001), congestive heart failure (aOR 1.34, 95% CI 1.01, 1.78; p = 0.043), tobacco smoking (aOR 1.48, 95% CI 1.23, 1.78; p < 0.019)] and hospitalization events [leukocytosis (aOR 1.64, 95% CI 1.32, 2.04; p < 0.001), hyponatremia (aOR 1.66, 95% CI 1.39, 1.98; p < 0.001), acute hypotension (aOR 1.67, 95% CI 1.31, 2.11; p < 0.001)] independently associated with the development of vasospasm. Intraparenchymal and subarachnoid hemorrhage were not associated with the development of vasospasm following multivariable adjustment. Among significant associations, a CHAID decision tree algorithm identified age 50-59 (parent node), hyponatremia, and leukocytosis as important determinants of vasospasm development. The cAVM-VPM achieved an area under the curve of 0.65 (sensitivity = 0.70, specificity = 0.53). Progression to DCI, but not vasospasm alone, was independently associated with in-hospital mortality (aOR 2.35, 95% CI 1.29, 4.31; p = 0.016) and lower likelihood of routine discharge (to home or to acute rehabilitation) (aOR 0.62, 95% CI 0.41, 0.96; p = 0.031) following adjustment for baseline covariates. Conclusion This population-based analysis of vasospasm in cAVM identifies common clinical risk factors for its development and establishes progression to DCI as a predictor of poor neurological outcomes.

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