1.Case analysis of hospitals′s infringement on patients′ right to informed consent from the perspective of the Civil Code of the People′s Republic of China
Linshan TANG ; Mengli TANG ; Lizhen YANG ; Xuejuan GAO
Chinese Journal of Hospital Administration 2024;40(8):640-646
Objective:To analyze the problems existing in the cases of hospitals infringing upon patients′ informed consent right after the promulgation of the Civil Code of the People′ s Republic of China, and to provide reference for improving the legal system of informed consent. Methods:Search for judgment documents published from January 1, 2021 to June 30, 2023 on the China Judgment Document Network using the keyword " liability dispute for infringing on patients′ informed consent rights", and conduct descriptive and textual analysis on the cases in the judgment documents.Results:68 judgment documents were included in total.There were 11 judgment documents on infringement of patients′ right to informed consent, and all related cases have undergone appraisal. The content of infringement mainly included infringement of patients′ right to know their condition (12/20), infringement of patients′ right to access their medical records (6/20), infringement of patients′ right to bodily integrity without consent (2/20). There were 15 judgment documents which judge that the right of informed consent of patients wasn′t infringed, and only one case in the document has been appraised. The main focus of controversy was the issue of the priority of the exercise of the right to informed consent (2/15), the fulfillment of the obligation to inform the right to informed consent (5/15), the issue of surgery without notification (1/15), and the issue of determining the authenticity of medical records and providing medical materials (7/15).Conclusions:The legal protection of patients′ right to informed consent still faces judicial difficulties such as unclear order of the exercise of rights subject, insufficient specificity of the scope of the exercise of the right, conflicts between the right to informed consent and medical intervention, and lack of unified identification methods for infringement liability. It is suggested to standardize the order of the exercise subject of the right to informed consent, clarify the content of the obligation of the medical party to inform, construct a system for medical intervention, and unify the identification methods for disputes related to the right to informed consent.
2.Effect of nonoperative treatment on the outcome of patients with posttraumatic hydrocephalus.
Linshan FU ; Yunhai TANG ; Shiyu WANG
Chinese Journal of Traumatology 2002;5(1):7-11
OBJECTIVETo compare the outcome of non-operative treatment with the outcome of surgical intraventricular drainage for patients with posttraumatic hydrocephalus including complications, mortality and favorable outcome.
METHODSThirty-nine patients were assigned to a nonoperative treatment group and 38 patents to a surgical intraventricular drainage group. Each patient's outcome was evaluated 3 years after treatment by using Glasgow Outcome Scale.
RESULTSIn the nonoperative treatment group the rate of favor able outcome (good recovery or mild disability) was 89.74% (35 of 39 patients) and the mortality was 2.56% (1 of 39 patients). In the surgical intraventricular drainage group the rate of favorable outcome was 71.05% (27 of 38 patients) and the mortality was 13.16% (5 of 38 patients; P<0.05). Mortality was not significantly different between the two groups.
CONCLUSIONSNonoperative treatment may be better than surgical intraventricular drainage for patients with posttraumatic hydrocephalus.
Adult ; Brain Injuries ; complications ; Chi-Square Distribution ; Female ; Humans ; Hydrocephalus ; etiology ; mortality ; therapy ; Male ; Treatment Outcome
3.The mechanism of hyperbaric oxygen regulating HMGB1 in the prevention and treatment of encephalopathy after acute CO poisoning
Linshan ZHAO ; Xing LIU ; Jiangwei TANG ; Yu GENG
Chinese Journal of Industrial Hygiene and Occupational Diseases 2020;38(9):641-645
Objective:To study the expression of high mobility group protein 1 (HMGB1) in the brain of rats after hyperbaric oxygen (HBO) treatment of acute carbon monoxide poisoning (DEACMP) , and to explore the mechanism of HBO in the prevention and treatment of DEACMP pathological process by regulating HMGB1.Methods:108 SD rats were randomly divided into control group (NC group) and co group (CO group) . HBO treatment group (HBO group) , 48 rats in each group. Co group and HBO group were used to establish CO poisoning model, HBO group were treated with hyperbaric oxygen once a day. Water maze test was used to detect and analyze the memory retention ability of three groups of rats in 3 d, 7 d, 14 d. ELISA was used to detect the plasma concentration of HMGB1、IL-6、TNF-α in three groups of rats on the 1 d, 3 d, 7 d, 14 d, 21 d Concentration. Western blotting was used to detect the expression of HMGB1 and Caspase-3 in the brain of the three groups on the 1 d, 3 d, 7 d, 14 d, 21 d. TUNEL staining was used to detect the apoptosis of hippocampal neurons in the three groups.Results:Compared with NC group, the average escape latency of rats in CO group and HBO group was significantly prolonged, and the activity time of platform quadrant in CO group was significantly shortened on 14 d and 21 d ( P<0.05) ; compared with CO group, the average escape latency of HBO group on 7 d, 14 d and 21 d was significantly shortened ( P<0.05) . Compared with NC group, plasma HMGB1 in CO group and HBO group were significantly increased ( P<0.05) ; after 3 days, HBO group was significantly lower than co group, the difference was statistically significant ( P<0.05) . The levels of IL-6 and TNF-α in HBO group and co group increased rapidly and then decreased gradually. The increased levels of IL-6 and TNF-α in HBO group were significantly lower than those in CO group ( P<0.05) . Compared with NC group, the expression of HMGB1 and Caspase-3 in CO group was significantly increased on 3 d, 7 d and 14 d ( P<0.05) ; the expression of HMGB1 and Caspase-3 in HBO group was significantly increased on 3 d, 7 d, 14 d and 21 d ( P<0.05) ; compared with CO group, the expression of HMGB1 and Caspase-3 in HBO group decreased significantly on 3 d, 7 d, 14 d and 21 d ( P<0.05) . The apoptotic index of nerve cells in CO group began to increase at 3 days, which was significantly different from that of NC group ( P<0.05) , and the difference was still statistically significant on 21 d ( P<0.05) ; the apoptotic index of nerve cells in HBO group was slightly increased, but there was no significant difference compared with NC group ( P>0.05) , and the apoptotic index of 3 d, 7 d, 14 d and 21 d in HBO group was significantly lower than that in CO group ( P<0.05) . Conclusion:acute CO poisoning can induce the release of HMGB1 and a variety of inflammatory factors. HMGB1 can promote the apoptosis of nerve cells after acute CO poisoning by up regulating the expression of caspase-3 protein, and participate in the pathological process of DEACMP. HBO can down regulate the expression of HMGB1, IL-6, TNF-α and caspase-3 protein, inhibit the apoptosis of nerve cells, and play a protective role on nerve cells.
4.The mechanism of hyperbaric oxygen regulating HMGB1 in the prevention and treatment of encephalopathy after acute CO poisoning
Linshan ZHAO ; Xing LIU ; Jiangwei TANG ; Yu GENG
Chinese Journal of Industrial Hygiene and Occupational Diseases 2020;38(9):641-645
Objective:To study the expression of high mobility group protein 1 (HMGB1) in the brain of rats after hyperbaric oxygen (HBO) treatment of acute carbon monoxide poisoning (DEACMP) , and to explore the mechanism of HBO in the prevention and treatment of DEACMP pathological process by regulating HMGB1.Methods:108 SD rats were randomly divided into control group (NC group) and co group (CO group) . HBO treatment group (HBO group) , 48 rats in each group. Co group and HBO group were used to establish CO poisoning model, HBO group were treated with hyperbaric oxygen once a day. Water maze test was used to detect and analyze the memory retention ability of three groups of rats in 3 d, 7 d, 14 d. ELISA was used to detect the plasma concentration of HMGB1、IL-6、TNF-α in three groups of rats on the 1 d, 3 d, 7 d, 14 d, 21 d Concentration. Western blotting was used to detect the expression of HMGB1 and Caspase-3 in the brain of the three groups on the 1 d, 3 d, 7 d, 14 d, 21 d. TUNEL staining was used to detect the apoptosis of hippocampal neurons in the three groups.Results:Compared with NC group, the average escape latency of rats in CO group and HBO group was significantly prolonged, and the activity time of platform quadrant in CO group was significantly shortened on 14 d and 21 d ( P<0.05) ; compared with CO group, the average escape latency of HBO group on 7 d, 14 d and 21 d was significantly shortened ( P<0.05) . Compared with NC group, plasma HMGB1 in CO group and HBO group were significantly increased ( P<0.05) ; after 3 days, HBO group was significantly lower than co group, the difference was statistically significant ( P<0.05) . The levels of IL-6 and TNF-α in HBO group and co group increased rapidly and then decreased gradually. The increased levels of IL-6 and TNF-α in HBO group were significantly lower than those in CO group ( P<0.05) . Compared with NC group, the expression of HMGB1 and Caspase-3 in CO group was significantly increased on 3 d, 7 d and 14 d ( P<0.05) ; the expression of HMGB1 and Caspase-3 in HBO group was significantly increased on 3 d, 7 d, 14 d and 21 d ( P<0.05) ; compared with CO group, the expression of HMGB1 and Caspase-3 in HBO group decreased significantly on 3 d, 7 d, 14 d and 21 d ( P<0.05) . The apoptotic index of nerve cells in CO group began to increase at 3 days, which was significantly different from that of NC group ( P<0.05) , and the difference was still statistically significant on 21 d ( P<0.05) ; the apoptotic index of nerve cells in HBO group was slightly increased, but there was no significant difference compared with NC group ( P>0.05) , and the apoptotic index of 3 d, 7 d, 14 d and 21 d in HBO group was significantly lower than that in CO group ( P<0.05) . Conclusion:acute CO poisoning can induce the release of HMGB1 and a variety of inflammatory factors. HMGB1 can promote the apoptosis of nerve cells after acute CO poisoning by up regulating the expression of caspase-3 protein, and participate in the pathological process of DEACMP. HBO can down regulate the expression of HMGB1, IL-6, TNF-α and caspase-3 protein, inhibit the apoptosis of nerve cells, and play a protective role on nerve cells.