Objective To provide information for the establishment of a medical risk monitoring and precaution system in China, by reviewing and analyzing the current status of medical risk management system and preventative measures in New Zealand, Methods We searched EI (1969-2006), SCI and SSCI (1975-2006), EMBASE (1966-2006), SCOPUS (included 100% MEDLINE) (1960-2006), VIP (1989-2006), CNKI (1979-2006) and relevant official and governmental websites. This search was conducted in January 2006 and articles about medical risk management and prevention were collected. Results We included 10 articles involving medical adverse events, patient safety and medical litigation. New Zealand took many measures in order to prevent medical error and improve medical quality, including strengthening medical practice standards, doctor-patient communication, safety awareness and promoting informationization of hospitals. New Zealand also revised “The Health Practitioners Competence Assurance Act” and improved medical litigation to form an appropriate law environment. Conclusions New Zealand has taken many measures and established a medical risk management system to prevent medical risk. Some issues of particular relevance to China include building corresponding medical litigation and relevant laws and regulations.
Objective To explore the protective effect and mechanism of Astragalus polysaccharides (APS) on liver injury in the state of brain death in New Zealand rabbits. Methods Twenty-four New Zealand rabbits were randomly divided into 3 groups (n=8): the blank control group, the brain death group, and the APS group. We obtained blood and liver tissue specimens from rabbits of three groups at 4 h and 8 h after treatment respectively (n=4). The rabbits of blank control group simulated the procedures of anesthesia and surgery of the brain death, without the Foley balloon catheter being pressurized, and maintained anesthesia. The brain death group: brain-dead models were established. The APS group: injection of APS (12 mg/kg) via the femoral vein bolus immediately after anesthesia, brain-dead models were established as same as rabbits of brain death group. The blood and liver tissue samples were taken at 4 h and 8 h after treatment to detect aminotrans-ferase (AST), alanine amino-transferase (ALT) and tumor necrosis factor α (TNF-α), and to observe the change of liver tissue by HE staining and immunohistochemical staining〔expression level of nuclear transcription factor p65 protein (NF-κB p65) could be detected by immunohistochemical staining〕. Results ① ALT and AST. Compare with the blank control group at the same time (4 h and 8 h), levels of ALT and AST in brain death group and APS group were significantly increased (P<0.05), and the levels of ALT and AST in brain death group were higher than those of APS group at each time point (P<0.05). In the same group, compared with 4 h, there was no significant difference in the levels of ALT and AST in blank control group at 8 h (P>0.05); the levels of ALT and AST in brain death group at 8 h were both higher than those of 4 h (P<0.05); the levels of ALT at 8 h in APS group was higher than that of 4 h, but there was no significant difference in the level of AST between 4 h and 8 h (P>0.05). ② TNF-α. Compare with the blank control groups at same time (4 h and 8 h), levels of TNF-α in brain death group and APS group were significantly increased(P<0.05), and level of TNF-α in brain death group was higher than that of APS group at 4 h and 8 h (P<0.05). ③ The HE results. The liver tissue structure of blank control group, brain death group, and APS group at 4 h had no obvious change. The liver tissue structure of brain death group at 8 h showed the evident tissue damage: liver cells showed the balloon samples, disordered arrangement, cytoplasmic loose light dye net-like, and inflammatory cells infiltrated in portal area. The liver tissue structure of APS group at 8 h showed that, liver cells showed mild edema, normal arrangement, and a small amount of inflammatory cells infiltrated in portal area. The liver tissue structure damage of APS group at 8 h was milder than that of brain death group. ④ Immunohistochemical staining results. There was no significant difference in expression levels of NF-κB p65 protein among blank control group, brain death group, and APS group at 4 h (P>0.05). But at 8 h, the expression levels of NF-κB p65 protein in brain death group and APS group were higher than that of blank control group (P<0.05), and the expression level of NF-κB p65 protein in brain death group was higher than that of APS group (P<0.05). The expression levels of NF-κB p65 protein in brain death group and APS group at 8 h was higher than that of 4 h in the same group (P<0.05), but there was no significant difference between 4 h and 8 h in blank control group (P>0.05). Conclusions Brain death will cause liver damage and the injury degree may be related to the continuous time. The damage at 8 h was more serious than that of 4 h. APS has a protective effect on liver of brain-dead rabbits' and its mechanism may be closely related to inhibit TNF-α and NF-κB by diverse ways to reduce the inflammation of the liver injury.