Review Articles

Decreased Cerebral Flow Velocities from General Anesthesia are Not Associated with Cerebral Hyperperfusion Syndrome

  • Yumei Liu, MD, PhD ,
  • Yang Hua, MD ,
  • Yabing Wang, MD, PhD ,
  • Nan Zhang, MS ,
  • Ting Ma, MD, PhD ,
  • Yue Zhao, MS ,
  • Na Li, MS ,
  • Na Lei, MS ,
  • Ran Liu, MS
Expand
  • a Department of Vascular Ultrasound, Xuanwu Hospital, Capital Medical University, Beijing, China
    b Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China
    c Department of Anesthesia, Xuanwu Hospital, Capital Medical University, Beijing, China
*Department of Vascular Ultrasound, Xuanwu Hospital, Capital Medical University, Beijing, 100045, China, e-mail: dryanghua99@163.com

Received date: 2022-08-24

  Revised date: 2023-10-16

  Accepted date: 2022-11-13

  Online published: 2023-10-09

Abstract

Objective: General anesthesia (GA) can decrease cerebral flow velocities and predispose patients to cerebral hyperperfusion syndrome (CHS) and other perioperative adverse events after carotid endarterectomy (CEA). The aim of this study was to investigate whether decreased pre-operative flow velocity is associated with an increased risk of CHS and perioperative cerebral infarct, and to further identify risk factors if there is any.
Methods: We retrospectively evaluated 920 consecutive patients who received CEA from 2010 to 2020 at a major academic hospital in China. Middle cerebral artery (MCA) blood flow velocities were measured before and after induction of the GA by transcranial Doppler (TCD). Patients were classified into two groups: the NORMAL group if flow velocity decreased<30% and the LOW group if flow velocity decreased ≥30%. The ultrasonographic diagnostic criterion of CHS was defined as the 100% increase in flow velocity by TCD from the baseline to post-CEA. The occurrence of CHS, perioperative cerebral infarction was compared between the two groups.
Results: 399 (43.4%) were classified as LOW measurement, and 521 (56.6%) patients were classified as NORMAL measurement. In the LOW group, there were more patients with diabetes, fewer patients with ipsilateral ICA severe stenosis and the opening of anterior/posterior communicating artery. Although the occurrence of CHS per ultrasonography criteria was higher in the LOW group (21.3% vs 15.7%, P = 0.03), the occurrence of CHS per clinical criteria (3.2%, vs 2.1%, P = 0.28) or the perioperative cerebral infarct between the two groups (5.8% vs 5.0%, P = 0.60) is equivalent.
Conclusion: Patients with decreased flow velocities post-GA were more likely to meet the ultrasonography criteria for CHS, but they are not at risk of developing clinical CHS or perioperative cerebral infarct.

Cite this article

Yumei Liu, MD, PhD , Yang Hua, MD , Yabing Wang, MD, PhD , Nan Zhang, MS , Ting Ma, MD, PhD , Yue Zhao, MS , Na Li, MS , Na Lei, MS , Ran Liu, MS . Decreased Cerebral Flow Velocities from General Anesthesia are Not Associated with Cerebral Hyperperfusion Syndrome[J]. ADVANCED ULTRASOUND IN DIAGNOSIS AND THERAPY, 2023 , 7(3) : 248 -253 . DOI: 10.37015/AUDT.2023.220032

References

[1] Radak D, de Waard D, Halliday A, Neskovic M, Tanaskovic S. Carotid endarterectomy has significantly lower risk in the last two decades: Should the guidelines now be updated? The Journal of cardiovascular surgery 2018; 59:586-599.
[2] van Mook WN, Rennenberg RJ, Schurink GW, van Oostenbrugge RJ, Mess WH, Hofman PA, et al. Cerebral hyperperfusion syndrome. The Lancet Neurology 2005; 4:877-888.
[3] Sundt Jr T, Sharbrough F, Piepgras D, Kearns T, Messick Jr J, O'fallon W. Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy, with results of surgery and hemodynamics of cerebral ischemia. Survey of Anesthesiology 1982; 26:200-201.
[4] Patel R, Turtle M, Chambers D, Newman S, Venn G. Hyperperfusion and cerebral dysfunction. Effect of differing acid-base management during cardiopulmonary bypass. European journal of cardio-thoracic surgery: official journal of the European Association for Cardio-thoracic Surgery 1992; 7:457-463; discussion 464.
[5] Sieskiewicz A, Lyson T, Drozdowski A, Piszczatowski B, Rutkowski R, Turek G, et al. Blood flow velocity in the middle cerebral artery during transnasal endoscopic skull base surgery performed in controlled hypotension. Neurologia i neurochirurgia polska 2014; 48:181-187.
[6] Newman J, Ali M, Sharpe R, Bown M, Sayers R, Naylor A. Changes in middle cerebral artery velocity after carotid endarterectomy do not identify patients at high-risk of suffering intracranial haemorrhage or stroke due to hyperperfusion syndrome. European Journal of Vascular and Endovascular Surgery 2013; 45:562-571.
[7] Fujimoto S, Toyoda K, Inoue T, Hirai Y, Uwatoko T, Kishikawa K, et al. Diagnostic impact of transcranial color-coded real-time sonography with echo contrast agents for hyperperfusion syndrome after carotid endarterectomy. Stroke 2004; 35:1852-1856.
[8] Iwata T, Mori T, Tajiri H, Nakazaki M. Predictors of hyperperfusion syndrome before and immediately after carotid artery stenting in single-photon emission computed tomography and transcranial color-coded real-time sonography studies. Neurosurgery 2011; 68:649-656.
[9] Tang SC, Huang YW, Shieh JS, Huang SJ, Yip PK, Jeng JS. Dynamic cerebral autoregulation in carotid stenosis before and after carotid stenting. Journal of vascular surgery 2008; 48:88-92.
[10] Franceschi M, Alberoni M, Bressi S, Canal N, Comi G, Fazio F, et al. Correlations between cognitive impairment, middle cerebral artery flow velocity and cortical glucose metabolism in the early phase of alzheimer’s disease. Dementia and Geriatric Cognitive Disorders 1995; 6:32-38.
[11] Chillon J, Baumbach G. Autoregulation: Arterial and intracranial pressure. Cerebral blood flow and metabolism. 2002; 2:395-412.
[12] Kim KH, Lee CH, Son YJ, Yang HJ, Chung YS, Lee SH. Post-carotid endarterectomy cerebral hyperperfusion syndrome: Is it preventable by strict blood pressure control? Journal of Korean Neurosurgical Society 2013; 54:159-163
[13] Stel?gowski M, Bogusiak K, Kasielska A, ?ysakowski M, Ka?mierski P, Szostek M. Intracranial occlusions and internal carotid artery stenoses: Clinical implications. Annals of vascular surgery 2010; 24:786-793.
[14] Ballotta E, Toniato A, Da Roit A, Baracchini C. Clinical outcomes of carotid endarterectomy in symptomatic and asymptomatic patients with ipsilateral intracranial stenosis. World Journal of Surgery 2015; 39:2823-2830.
[15] Han Y, Park H, Kwon SU, Kang DW, Lee DH, Kwon H, et al. Clinical outcomes of carotid endarterectomy in patients with carotid artery tandem lesions. Stroke 2014; 45:3443-3446.
[16] Beckman JA, Creager MA, Libby P. Diabetes and atherosclerosis: Epidemiology, pathophysiology, and management. JAMA 2002; 287:2570-2581.
[17] Marmarelis V, Mitsis G, Shin D, Zhang R. Multiple-input nonlinear modelling of cerebral haemodynamics using spontaneous arterial blood pressure, end-tidal co2 and heart rate measurements. Phil. Trans. R. Soc. A 2016; 374:20150180.
[18] Baumgartner R. Intracranial stenoses and occlusions, and circle of willis collaterals. Handbook on neurovascular ultrasound Karger Publishers; 2006:117-126.
[19] Kennedy McConnell F, Payne S. The dual role of cerebral autoregulation and collateral flow in the circle of willis after major vessel occlusion. IEEE transactions on bio-medical engineering 2016.
[20] Ogasawara K, Inoue TM, Endo H, Yoshida K, Fukuda T, Terasaki K, et al. Cerebral hyperperfusion following carotid endarterectomy: Diagnostic utility of intraoperative transcranial doppler ultrasonography compared with single-photon emission computed tomography study. American Journal of Neuroradiology 2005; 26:252-257.
Outlines

/