Development of cerebral vasospasm following traumatic intracranial hemorrhage: incidence, risk factors, and clinical outcomes

Abstract

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.

Incidence, risk factors, and clinical outcomes of acute brain swelling associated with traumatic acute subdural hematoma: a retrospective study utilizing novel diagnostic criteria

“…SAH is characterized by bleeding in the subarachnoid space that can result in the release of neuroinflammatory substances and subsequent cerebral vasospasm. 17 Previous studies have suggested that the mechanisms of vasospasm following traumatic SAH may be similar to those identified in aneurysmal SAH. 18 In non-traumatic SAH, the occurrence of vasospasm typically presents a significant delay and is associated with delayed cerebral ischemia and subsequent elevated ICP.…”

Cerebral vasospasm following arteriovenous malformation rupture: a population-based cross-sectional study

“…35,36 These ICD codes do not carry a temporal qualifier, meaning that their occurrence with respect to vasospasm (before or after) cannot be ascertained, which limits conclusions regarding causality. 11 The inability of the NIS to accurately identify vasospasm and DCI and to differentiate these entities from ischemia and infarction due to the mass effect from hematoma expansion, increased intracranial pressure, or iatrogenic causes may have led to overreporting and a potential type I error. Moreover, the degree, time, and location of arterial vasospasm could not be identified.…”

“…Diagnosis of cerebral vasospasm (ICD-10-CM I67.84) was made in accordance with previous literature. 10,11 To ensure that radiographic evidence was used for the identification of patients experiencing vasospasm, only patients receiving diagnostic cerebral angiograms (ICD-10-PCS B31XXXX) during their hospitalization were included in the analysis. Delayed cerebral ischemia (DCI) was defined as the concurrent coding of cerebral vasospasm and cerebral infarction due to nonthromboembolic and noniatrogenic causes (ICD-10-CM I63.5).…”

Neurovascular Interventions for Neurotrauma: From Treatment of Injured Vessels to Treatment of the Injured Brain?

“…With growing operators' experience in using these devices, their use has slowly expanded in an off-label manner into the treatment of a wide range of arterial injuries requiring vessel reconstruction. 26 Promising results with flow diversion have been shown for delayed cerebrovascular pathology including pseudoaneurysms 4,27 (especially at the cervical carotid), arteriovenous fistulae (such as carotid-cavernous fistulae, CCF), 28 and dissections 6 (see Figure 1).…”

“…[3][4][5] Neurovascular pathologies are better diagnosed today because imaging studies have improved. Recent advancements in endovascular neurosurgery enable accurate and effective vessel reconstruction/deconstruction techniques, which can contribute to the management of such injuries, 6 and many additional new applications for the treatment of brain-injured patients are being explored. [7][8][9][10][11] A rapidly evolving field, endovascular neurosurgery, is now explored as a route of delivery of treatment for brain tumors, CSF, and movement disorders.…”