Systemic Hemodynamic Changes in Low-Dose Ethanol Embolotherapy for Soft-Tissue Arteriovenous Malformations

• 来源期刊: 中国整形与重建外科（英文）
• 年，卷（期）: 2021,（1）
• 所属期刊栏目: Original Article
• 页码范围: 32-40
• 页数: 9页
• 语种: 中文

摘要

Background Ethanol embolotherapy is considered an optimal choice for the treatment of arteriovenous malformations (AVMs); however, there are some complications associated with this treatment. This study aimed to prospectively investigate systemic hemodynamic changes in high-flow AVMs using ethanol embolotherapy. Methods From September 2012 to September 2014, 34 male patients and 26 female patients with AVMs who underwent embolotherapy (100 sessions in total) with absolute ethanol were included in this study. Invasive systolic blood pressure (SBP) and heart rate (HR) were recorded before and after each injection and throughout the procedure. Differences between the initial and highest SBP (?maxSP) and HR values (?maxHR), as well as the initial and final SBP (?SP) and HR (?HR) values, were analyzed. We aimed to explore the potential association between these values and the amount of ethanol that was used. Results The total ethanol used was variable (0.01–0.40 mL/kg; mean, 0.20 mL/kg). SBP and HR increased after ethanol injection in most sessions (91 in 100 sessions). SBP decreased in 9 sessions (9 in 100 sessions), while HR, oxygen saturation, and end-tidal CO2 decreased in one of the 9 sessions. ?maxSP and ?maxHR averaged 38.4 mmHg and 27.8 bpm, respectively (both P<0.05), while ?SP and ?HR averaged 3.4 mmHg and 4.0 bpm, respectively (both P<0.05). ?maxSP and ?maxHR were positively correlated with the total dose of ethanol injected. Conclusions Elevations in SBP and HR during ethanol embolotherapy are common, temporary, and most likely pain-mediated; these increases tend to be positively correlated with ethanol dose. Hypotension may be regarded as an acute complication of ethanol embolotherapy. Hypotension combined with bradycardia, oxygen desaturation, and decreased end-tidal CO2 may be a potential predictor of cardiovascular collapse.