Fiani Brian, Fowler James B, Figueras Ryan Arthur, Hessamian Keon, Mercado Nathan, Vukcevich Olivia, Singh Manpreet Kaur
Department of Neurosurgery, Desert Regional Medical Center, Palm Springs, United States.
School of Medicine, University of California Riverside, Riverside, California, United States.
Surg Neurol Int. 2021 Apr 26;12:187. doi: 10.25259/SNI_214_2021. eCollection 2021.
The novel severe acute respiratory syndrome coronavirus 2 is responsible for over 83 million cases of infection and over 1.8 million deaths since the emergence of the COVID-19 pandemic. Because COVID-19 infection is associated with a devastating mortality rate and myriad complications, it is critical that clinicians better understand its pathophysiology to develop effective treatment. Cumulative evidence is suggestive of cerebral aneurysms being intertwined with the hyperinflammatory state and hypercytokinemia observed in severe COVID-19 infections.
In case example 1, the patient presents with chills, a mild cough, and sore throat. The patient develops high-grade fever of 39.8° C, decreased oxygen saturation of 93% on room air, and an extensive spontaneous subarachnoid hemorrhage (SAH) in the basal cisterns from a ruptured left posterior communicating artery aneurysm. In case example 2, the patient presents with a positive PCR test for COVID-19 2 weeks prior with spontaneous SAH and found to have a large multilobulated bulbous ruptured aneurysm of the anterior communicating artery. Both patients' symptoms and high-grade fever are consistent with hypercytokinemia and a hyperinflammatory state, with elevated granulocyte colony-stimulating factor, inducible protein-10, monocyte chemoattractant protein-1, M1P1A, and tumor necrosis factor-α inflammatory mediators found to be elevated in COVID-19 intensive care unit admissions.
COVID-19 effect on cerebral aneurysms requires future studies to clearly delineate correlation, however, hypercytokinemia and a hyperinflammatory state are strongly implicated to cause degenerative vascular changes that may predispose patients to cerebral aneurysm formation, change in size or morphology, and resultant aneurysm rupture.
自新型冠状病毒肺炎疫情出现以来，新型严重急性呼吸综合征冠状病毒2已导致超过8300万例感染和超过180万人死亡。由于新型冠状病毒肺炎感染与极高的死亡率和众多并发症相关，临床医生更好地了解其病理生理学以制定有效的治疗方法至关重要。越来越多的证据表明，脑动脉瘤与重症新型冠状病毒肺炎感染中观察到的高炎症状态和高细胞因子血症相互关联。
在病例1中，患者出现寒战、轻度咳嗽和咽痛。患者体温高达39.8℃，在室内空气中氧饱和度降至93%，因左侧后交通动脉瘤破裂导致基底池广泛自发性蛛网膜下腔出血（SAH）。在病例2中，患者2周前新型冠状病毒肺炎核酸检测呈阳性，伴有自发性SAH，发现前交通动脉有一个巨大的多叶球状破裂动脉瘤。两名患者的症状和高热均与高细胞因子血症和高炎症状态一致，在新型冠状病毒肺炎重症监护病房入院患者中发现粒细胞集落刺激因子、诱导蛋白-10、单核细胞趋化蛋白-1、M1P1A和肿瘤坏死因子-α等炎症介质升高。
新型冠状病毒肺炎对脑动脉瘤的影响需要未来的研究来明确界定相关性，然而，高细胞因子血症和高炎症状态被强烈认为会导致血管退行性改变，这可能使患者易患脑动脉瘤形成、大小或形态改变以及由此导致的动脉瘤破裂。
