Liotta Eric M, Lizza Bryan D, Romanova Anna L, Guth James C, Berman Michael D, Carroll Timothy J, Francis Brandon, Ganger Daniel, Ladner Daniela P, Maas Matthew B, Naidech Andrew M
1Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL.2Department of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, IL.3Department of Radiology, Feinberg School of Medicine, Northwestern University, Chicago, IL.4Division of Gastroenterology and Hepatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL.5Division of Surgery-Organ Transplantation, Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL.
Crit Care Med. 2016 Jan;44(1):171-9. doi: 10.1097/CCM.0000000000001276.
Cerebral edema is common in severe hepatic encephalopathy and may be life threatening. Bolus 23.4% hypertonic saline improves surveillance neuromonitoring scores, although its mechanism of action is not clearly established. We investigated the hypothesis that bolus hypertonic saline decreases cerebral edema in severe hepatic encephalopathy utilizing a quantitative technique to measure brain and cerebrospinal fluid volume changes.
Retrospective analysis of serial CT scans, and clinical data for a case-control series were performed.
ICUs of a tertiary care hospital.
Patients with severe hepatic encephalopathy treated with 23.4% hypertonic saline and control patients who did not receive 23.4% hypertonic saline.
23.4% hypertonic saline bolus administration.
We used clinically obtained CT scans to measure volumes of the ventricles, intracranial cerebrospinal fluid, and brain using a previously validated semiautomated technique (Analyze Direct, Overland Park, KS). Volumes before and after 23.4% hypertonic saline were compared with Wilcoxon signed rank test. Associations among total cerebrospinal fluid volume, ventricular volume, serum sodium, and Glasgow Coma Scale scores were assessed using Spearman rank correlation test. Eleven patients with 18 administrations of 23.4% hypertonic saline met inclusion criteria. Total cerebrospinal fluid (median, 47.6 mL [35.1-69.4 mL] to 61.9 mL [47.7-87.0 mL]; p < 0.001) and ventricular volumes (median, 8.0 mL [6.9-9.5 mL] to 9.2 mL [7.8-11.9 mL]; p = 0.002) increased and Glasgow Coma Scale scores improved (median, 4 [3-6] to 7 [6-9]; p = 0.008) after 23.4% hypertonic saline. In contrast, total cerebrospinal fluid and ventricular volumes decreased in untreated control patients. Serum sodium increase was associated with increase in total cerebrospinal fluid volume (r = 0.83, p < 0.001), and change in total cerebrospinal fluid volume was associated with ventricular volume change (r = 0.86; p < 0.001).
Total cerebrospinal fluid and ventricular volumes increased after 23.4% hypertonic saline, consistent with a reduction in brain tissue volume. Total cerebrospinal fluid and ventricular volume change may be useful quantitative measures to assess cerebral edema in severe hepatic encephalopathy.
脑水肿在严重肝性脑病中很常见,可能危及生命。静脉推注23.4%高渗盐水可改善监测神经监测评分,但其作用机制尚未明确确立。我们研究了以下假设:静脉推注高渗盐水可减轻严重肝性脑病中的脑水肿,采用定量技术测量脑和脑脊液体积变化。
对系列CT扫描及病例对照系列的临床数据进行回顾性分析。
一家三级护理医院的重症监护病房。
接受23.4%高渗盐水治疗的严重肝性脑病患者和未接受23.4%高渗盐水治疗的对照患者。
静脉推注23.4%高渗盐水。
我们使用临床获得的CT扫描,采用先前验证的半自动技术(Analyze Direct,堪萨斯州欧弗兰帕克)测量脑室、颅内脑脊液和脑的体积。使用Wilcoxon符号秩检验比较23.4%高渗盐水治疗前后的体积。使用Spearman秩相关检验评估总脑脊液体积、脑室体积、血清钠和格拉斯哥昏迷量表评分之间的关联。11例接受18次23.4%高渗盐水注射的患者符合纳入标准。23.4%高渗盐水治疗后,总脑脊液(中位数,47.6 mL[35.1 - 69.4 mL]至61.9 mL[47.7 - 87.0 mL];p < 0.001)和脑室体积(中位数,8.0 mL[6.9 - 9.5 mL]至9.2 mL[7.8 - 11.9 mL];p = 0.002)增加,格拉斯哥昏迷量表评分改善(中位数,4[3 - 6]至7[6 - 9];p = 0.008)。相比之下,未治疗的对照患者的总脑脊液和脑室体积减小。血清钠升高与总脑脊液体积增加相关(r = 0.83,p < 0.001),总脑脊液体积变化与脑室体积变化相关(r = 0.86;p < 0.001)。
23.4%高渗盐水治疗后,总脑脊液和脑室体积增加,这与脑组织体积减少一致。总脑脊液和脑室体积变化可能是评估严重肝性脑病中脑水肿的有用定量指标。