Abstract

Background: Cerebral vasospasm following tumour craniotomy (CVACT) is a rarely reported yet potentially devastating postoperative complication with significant neurological consequences. Unlike cerebral vasospasm associated with aneurysmal subarachnoid haemorrhage, which has been extensively studied, CVACT remains poorly understood with respect to its pathophysiology, early detection, and management. This lack of clarity often leads to delayed diagnosis and suboptimal therapeutic strategies. In this chapter, we present a comprehensive synthesis of the current literature, drawing upon published case reports and case series to identify emerging clinical patterns, key risk factors, available diagnostic approaches, and therapeutic responses associated with CVACT. The objective is to consolidate and interpret existing evidence regarding predisposing factors, potential underlying mechanisms, clinical presentation, diagnostic modalities, treatment strategies, and patient outcomes, thereby improving clinical awareness and informing future research directions. Methods: A systematic review was conducted in accordance with the PRISMA 2020 guidelines, utilising the PubMed and ScienceDirect databases. This review employed a Boolean combination of the MeSH terms and keywords "cerebral vasospasm," "craniotomy," and "brain tumour" to identify instances of cerebral vasospasm following tumour craniotomy (CVACT). The study protocol, which outlines the methodologies used in the systematic review, has been registered with the PROSPERO database. The inclusion criteria for this review consisted of case reports and case series published in English and available in full text, with no restrictions on publication year. Furthermore, gray literature was not excluded from the review. The final search was completed in May 2024. Results: We included 60 inclusion patients from 14 case reports and 13 case series, with 33 (55%) females and 27 (45%) males, with a mean age of 44.05 ± 16.8 years. The most common tumours were pituitary adenomas, which were found in 22 (36.66%). The most common tumour location was the middle cranial fossa (75%), and the most common surgery technique used was transsphenoidal surgery (50%). Most of those who experience vasospasm have a craniotomy with the TSS technique (50%), with complications of intraoperative bleeding. The range of onset of VS symptoms postoperatively was 0–30 days (mean 6.59d). The symptoms included asymptomatic, headache, loss of vision, hemiparesis, diplopia, etc. The vascular involvement was mainly anterior circulation (78.33%). The diagnostic tools most commonly used were angiography and transcranial doppler (TCD). The most common management of VS from the included studies was pharmacology. The survival rate was 61.66%. We found that the tumour location and vascular-affected vasospasm were significantly correlated with mortality rates: p = 0.015 and p = 0.02. Conclusions: Cerebral vasospasm after craniotomy tumour removal (CVACT) frequently arises in tumours situated in the medial cranial fossa, predominantly pituitary adenomas and meningiomas. The minimally invasive surgical approach of TSS may contribute to the mechanism of CVACT incidence. The existence of preoperative vascular pathology, such as encasement or narrowing, appears to be a predictor alongside the incidence of intra- or postoperative haemorrhage. The vascular structures most susceptible to vasospasm are located in the anterior circulation of the Willis circle, which appears to correlate with the vascular problems that typically undergo preoperative encasement of the internal carotid artery (ICA). The most reliable and real-time diagnostic instrument employed is TCD, while imaging continues to be the gold standard. Nimodipine treatment continues to be a viable therapeutic option that can enhance patient outcomes.

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