目的:探讨心脏外科术后患者出现低三碘甲状腺原氨酸（T3）综合征[即正常甲状腺功能病态综合征（ESS）]的影响因素。方法:选取2022年4月至8月于南京市第一医院接受体外循环（CPB）的354例心脏外科手术的成年心脏病患者作为研究对象，根据术后游离三碘甲状腺原氨酸（FT3）水平分为ESS组（FT3 < 2.43 pmol/L，64例）及非ESS组（FT3 ≥ 2.43 pmol/L，290例）。比较两组患者的临床资料，术前血生化、血常规指标及术后乳酸水平，分析影响心脏外科术后患者出现低T3综合征的危险因素。结果:与非ESS组患者比较，ESS组患者的年龄较高[（63 ± 11）岁vs.（66 ± 8）岁，t = 2.904，P = 0.004]，手术时间较长[（4.4 ± 1.1）h vs.（4.8 ± 1.2）h，t = 2.131，P = 0.034]，急性病生理学和长期健康评价（APACHE）Ⅱ评分较高[（12 ± 3）分vs.（14 ± 3）分，t = 3.613，P < 0.001]、糖尿病[19.66%（57/290）vs. 31.25%（20/64），χ2 = 4.141，P = 0.042]及冠状动脉粥样硬化性心脏病（CHD）[48.28%（140/290）vs. 70.31%（45/64），χ2 = 10.205，P = 0.001]占比均较高，术前白蛋白[（40 ± 3）g/L vs.（38 ± 3）g/L，t = 2.229，P = 0.026]及血红蛋白（HGB）[（130 ± 17）g/L vs.（125 ± 19）g/L，t = 2.358，P = 0.019]水平均显著降低。Logistic回归分析显示，APACHEⅡ评分[比值比（OR）= 1.180，95%置信区间（CI）（1.012，1.376），P = 0.035]是心脏术后患者并发低T3综合征的危险因素，而HGB[OR = 0.966，95% CI（0.938，0.995），P = 0.023]为其保护因素。结论:年龄、手术时间、APACHEⅡ评分、糖尿病、CHD、白蛋白及HGB水平与心脏外科术后出现低T3综合征密切相关。APACHEⅡ评分是心脏术后患者并发低T3综合征的危险因素，而HGB为其保护因素。
Chiari畸形又称为Arnold-Chiari畸形，是一种先天性颅颈交界区畸形疾病，以小脑扁桃体下疝为主要特征[1]。Chiari畸形患者的小脑扁桃体下疝压迫延髓，是引起中枢性呼吸暂停的危险因素，如不能做好及时的识别与精准化的复杂管理，则可能危及患者生命[2]。目前Chiari畸形主要分为4种类型[3]，其中合并颈髓弯曲、齿状突内陷、不正常的斜坡颈椎角、寰枢椎融合、颅底凹陷症等，被称为复杂的Chiari畸形。外科手术是临床治疗Chiari畸形的首选方法，尤其是合并寰椎枕骨关节、寰椎枢椎关节不稳定者，后颅窝减压术联合枕颈融合术能够有效恢复寰椎枕骨关节、寰椎枢椎关节稳定性[4]。临床上Chiari畸形合并颅底凹陷、脊柱侧弯且同时累及全段脊髓的空洞症病例较为罕见。2021年8月16日浙江大学医学院附属第一医院收治1例复杂Chiari畸形合并全脊髓空洞的患者，经多学科联合下的手术治疗和精心护理，患者病情好转，并于入院后第57天病情平稳出院。
脓毒症被定义为宿主对感染反应失调引起的危及生命的器官功能障碍[1]，具有较高的发病率和病死率，严重影响危重期患者的生命健康，增加患者的心理及经济负担，导致远期预后不良。据《全球疾病负担研究》估计，2017年脓毒症导致的死亡占全球可预防死亡的近20%[2]。其中，肾脏是脓毒症最常累及的器官之一，大约有60%的脓毒症患者伴发急性肾损伤（acute kidney injury，AKI）。当合并AKI时，脓毒症患者的病死率显著升高[3-4]。同时，与其他原因引起的AKI相比，脓毒症相关急性肾损伤（sepsis associated acute kidney injury，S-AKI）往往预后更差[5]。如未及时识别和处理S-AKI，患者将有可能发展成慢性肾脏病，增加心血管并发症的风险[6]。
Objective:To explore the effect of low-intensity inspiratory muscle training on mechanically ventilated patients.Methods:Eighty-one mechanically ventilated patients admitted to the intensive care unit and high dependency unit of the General Hospital of Southern Theatre Command from March 2020 to June 2022 were selected and randomly divided into a control group (41 patients) and an experimental group (40 patients). Six patients were lost to follow-up in the control group and four patients were lost in the experimental group during the trial, and finally 35 patients and 36 patients were included in the two groups, respectively. The control group was treated with conventional therapy, and the experimental group added inspiratory muscle training with 20% maximal inspiratory pressure (MIP) as the starting threshold load to the conventional therapy. After eight weeks of training, patients were assessed for the MIP, change in exertion spirometry, diaphragm thickness, diaphragm mobility, reintubation rate, in-hospital mortality, and quality of life.Results:After eight weeks of training, the MIP [(29.6 ± 4.8) cmH2O vs. (20.3 ± 5.5) cmH2O, t = 6.402, P < 0.001], exertional lung volume [(1 768 ± 655) mL vs. (1 420 ± 420) mL, t = 4.303, P < 0.001], diaphragm mobility [(0.93 ± 0.44) cm vs. (0.79 ± 0.32) cm, t = 2.313, P = 0.023], and modified Barthel index [15 (5, 19) vs. 10 (2, 14), U = 325.500, P = 0.040] of patients in the experimental group were significantly improved compared with the control group. The diaphragm thickness [(1.47 ± 0.38) mm vs. (1.39 ± 0.45) mm, t = 1.195, P = 0.236], reintubation rate [8.3% (3/36) vs. 11.4% (4/35), P = 0.520], and in-hospital mortality [8.3% (3/36) vs. 5.7% (2/35), P = 0.674] were not statistically significantly different between the experimental and control groups.Conclusion:Low-intensity inspiratory muscle training can significantly improve MIP and exertion spirometry, and may improve diaphragm mobility and quality of life in mechanically ventilated patients.
Objective:To explore the protective effect and mechanism of sodium butyrate on cardio-brain injury after cardiopulmonary resuscitation in pigs.Methods:A total of 24 large white healthy male pigs were divided into a sham operation group (n = 6), a cardiopulmonary resuscitation group (n = 10) and a sodium butyrate group (n = 8) by a random number method. In the sham operation group, only tracheal intubation and arteriovenous catheterization were performed, and induced ventricular fibrillation and cardiopulmonary resuscitation were not performed. Cardiac arrest and cardiopulmonary resuscitation models were prepared by electrical stimulation for 9 min and cardiopulmonary resuscitation for 6 min. At 5 min after successful resuscitation, the sodium butyrate group was injected 75 mg/kg of sodium butyrate through the femoral vein for 1 h. Sham operation and cardiopulmonary resuscitation groups were given the same amount of isotonic NaCl solution by the same method. Serum levels of cardiac troponin I (cTnI), creatine kinase MB (CK-MB), neuron specific enolase (NSE) and S100 calcium-binding protein B (S100B) were measured by the enzyme-linked immunosorbent assay (ELISA) before cardiac arrest and at 1, 2, 4, and 24 h after resuscitation. At 24 h after resuscitation, the expression levels of microtubule-associated protein 1 light chain 3 (LC3) and ubiquitin-binding protein 62 (p62) in the cardiac muscle and cerebral cortex tissue were detected by western-blotting, and the apoptosis rate was detected by the TUNEL method.Results:In the cardiopulmonary resuscitation group, nine pigs were successfully resuscitated, seven of which survived to 24 h. In the sodium butyrate group, seven pigs were resuscitated successfully, and all survived to 24 h. There was no significant difference in the success of 24-h resuscitation among the three groups (χ2 = 3.381, P = 0.184). At 1, 2, 4 and 24 h after resuscitation, serum cTnI (F = 62.736, 201.265, 330.083, 643.538; all P < 0.001), CK-MB (F = 90.380, 181.548, 669.657, 707.485; all P < 0.001), NSE (F = 92.302, 125.730, 590.627, 1 130.372; all P < 0.001) and S100B (F = 42.831, 152.004, 295.517, 1 023.409; all P < 0.001) were observed and compared in the three groups, and the differences were statistically significant. Compared with the sham operation group, the cTnI, CK-MB, NSE and S100B levels in serum were significantly increased at 2, 4 and 24 h after resuscitation in the cardiopulmonary resuscitation group and sodium butyrate group, which were highest in the cardiopulmonary resuscitation group (all P < 0.05). At 24 h after resuscitation, the levels of autophagy markers LC3 (F = 81.671, 49.204; both P < 0.001) and p62 (F = 127.620, 65.594; both P < 0.001) and the apoptosis rate (F = 116.750, 249.105; both P < 0.001) in cardiomyocytes and cerebral cortex cells were observed and compared in the three groups, and the differences were statistically significant. Compared with the sham operation group, the LC3 expression and apoptosis index were increased, and the p62 expression was decreased in myocardium and cerebral cortex of pigs in the cardiopulmonary resuscitation group and sodium butyrate group at 24 h after resuscitation (all P < 0.05). However, compared with the cardiopulmonary resuscitation group, the LC3 expression and apoptosis index were decreased, and the p62 expression was increased in the myocardium and cerebral cortex in the sodium butyrate group at 24 h after resuscitation (all P < 0.05).Conclusion:Sodium butyrate has a protective effect on cardio-brain injury after resuscitation of cardiac arrest, and the mechanism may be related to inhibition of autophagy and apoptosis.
