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Introduction Acute respiratory distress syndrome (ARDS) is a known predictor of poor outcomes in critically ill patients. We sought to examine the role ARDS plays in outcomes in subarachnoid hemorrhage (SAH) patients. Prior studies investigating the incidence of ARDS in SAH patients did not control for SAH severity. Hence, we sought to determine the incidence ARDS in patients diagnosed with aneurysmal SAH and investigate the predisposing risk factors and impact upon outcomes. Methods A retrospective cohort study was conducted using the National Inpatient Sample (NIS) database for the years 2008 to 2014. Multivariate stepwise regression analysis was performed to identify the risk factors and outcome associated with developing ARDS in the setting of SAH. Results We identified 170,869 patients with non-traumatic subarachnoid hemorrhage, of whom 6962 were diagnosed with ARDS and of those 4829 required mechanical ventilation. ARDS more frequently developed in high grade SAH patients (1.97 ± 0.05 vs. 1.15 ± 0.01; p Conclusion Patients with SAH who developed ARDS were less likely to be discharged home, more likely to need rehabilitation and had a significantly higher risk of mortality. The identification of risk factors contributing to ARDS is helpful for improving outcomes and resource utilization.

BACKGROUND Cerebral vasospasm is an alarming complication of acute bacterial meningitis with potentially devastating consequences. It is essential for providers to recognize and treat it appropriately. Unfortunately, there is no well-established approach to the management of postinfectious vasospasm, which makes it especially challenging to treat these patients. More research is needed to address this gap in care. OBSERVATIONS Here, the authors describe a patient with postmeningitis vasospasm that was refractory to induced hypertension, steroids, and verapamil. He eventually responded to a combination of intravenous (IV) and intra-arterial (IA) milrinone followed by angioplasty. LESSONS To our knowledge, this is the first report of successfully using milrinone as vasodilator therapy in a patient with postbacterial meningitis-associated vasospasm. This case supports the use of this intervention. In future cases of vasospasm after bacterial meningitis, IV and IA milrinone should be trialed earlier with consideration of angioplasty.

OBJECTIVE Studies examining the risk factors and clinical outcomes of arterial vasospasm secondary to cerebral arteriovenous malformation (cAVM) rupture are scarce in the literature. The authors used a population-based national registry to investigate this largely unexamined clinical entity. METHODS Admissions for adult patients with cAVM ruptures were identified in the National Inpatient Sample during the period from 2015 to 2019. 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 7215 cAVM patients identified, 935 developed vasospasm, corresponding to an incidence rate of 13.0%; 110 of these patients (11.8%) subsequently progressed to delayed cerebral ischemia (DCI). Multivariable adjusted modeling identified the following baseline clinical covariates: decreasing age by decade (adjusted odds ratio [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], and 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 years (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 (aOR 0.62, 95% CI 0.41–0.96; p = 0.031). CONCLUSIONS This large-scale assessment of vasospasm in cAVM identifies common clinical risk factors and establishes progression to DCI as a predictor of poor neurological outcomes.

OBJECTIVE Limited evidence exists characterizing the incidence, risk factors, and clinical associations of cerebral vasospasm following traumatic intracranial hemorrhage (tICH) on a large scale. Therefore, the authors sought to use data from a national inpatient registry to investigate these aspects of posttraumatic vasospasm (PTV) to further elucidate potential causes of neurological morbidity and mortality subsequent to the initial insult. METHODS Weighted discharge data from the National (Nationwide) Inpatient Sample from 2015 to 2018 were queried to identify patients with tICH who underwent diagnostic angiography in the same admission and, subsequently, those who developed angiographically confirmed cerebral vasospasm. Multivariable logistic regression analysis was performed to identify significant associations between clinical covariates and the development of vasospasm, and a tICH vasospasm predictive model (tICH-VPM) was generated based on the effect sizes of these parameters. RESULTS Among 5880 identified patients with tICH, 375 developed PTV corresponding to an incidence of 6.4%. Multivariable adjusted modeling determined that the following clinical covariates were independently associated with the development of PTV, among others: age (adjusted odds ratio [aOR] 0.98, 95% CI 0.97–0.99; p < 0.001), admission Glasgow Coma Scale score < 9 (aOR 1.80, 95% CI 1.12–2.90; p = 0.015), intraventricular hemorrhage (aOR 6.27, 95% CI 3.49–11.26; p < 0.001), tobacco smoking (aOR 1.36, 95% CI 1.02–1.80; p = 0.035), cocaine use (aOR 3.62, 95% CI 1.97–6.63; p < 0.001), fever (aOR 2.09, 95% CI 1.34–3.27; p = 0.001), and hypokalemia (aOR 1.62, 95% CI 1.26–2.08; p < 0.001). The tICH-VPM achieved moderately high discrimination, with an area under the curve of 0.75 (sensitivity = 0.61 and specificity = 0.81). Development of vasospasm was independently associated with a lower likelihood of routine discharge (aOR 0.60, 95% CI 0.45–0.78; p < 0.001) and an extended hospital length of stay (aOR 3.53, 95% CI 2.78–4.48; p < 0.001), but not with mortality. CONCLUSIONS This population-based analysis of vasospasm in tICH has identified common clinical risk factors for its development, and has established an independent association between the development of vasospasm and poorer neurological outcomes.