中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2011年
3期
173-175
,共3页
党伟%张宪%姚咏明%苏琴%果应菲%孙荣距%秦宇红%马俊勋%赵晓东
黨偉%張憲%姚詠明%囌琴%果應菲%孫榮距%秦宇紅%馬俊勛%趙曉東
당위%장헌%요영명%소금%과응비%손영거%진우홍%마준훈%조효동
严重创伤%胰岛素强化治疗%高迁移率族蛋白B1%预后
嚴重創傷%胰島素彊化治療%高遷移率族蛋白B1%預後
엄중창상%이도소강화치료%고천이솔족단백B1%예후
Severe trauma%Intensive insulin therapy%High mobility group box 1%Prognosis
目的 观察早期胰岛素强化治疗严重创伤后血清高迁移率蛋白B1(HMGB1)水平的变化,并探讨其与患者预后的关系.方法 将80例严重创伤患者[创伤严重度评分(ISS)≥16分]根据最重损伤解剖部位近似原则配对分组.强化治疗组(40例)早期即给予胰岛素强化治疗;常规治疗组(40例)根据临床经验给予常规胰岛素治疗.记录患者治疗72 h内胰岛素用量及血糖水平;于治疗后24、36、48、60、72 h检测血清HMGB1水平;记录1周内相关终点事件[包括多器官功能障碍综合征(MODS)、死亡];并分析HMGB1水平与预后的关系.结果 治疗72 h内强化治疗组胰岛素用量明显大于常规治疗组,血糖水平明显低于常规治疗组.强化治疗组治疗36 h时HMGB1水平有所下降,且36、48、60、72 h时HMGB1水平(μg/L)明显低于常规治疗组(36 h:41.3±9.5比52.7±11.5,48 h:48.6±17.6比124.1±22.9,60 h:47.7±23.3比132.9±33.4,72 h:54.3±26.3比140.6±16.5,P<0.05或P<0.01).强化治疗组MODS发生率和病死率均明显低于常规治疗组(20.0%比55.0%,10.0%比30.0%,均P<0.05).常规治疗组内HMGB1≥132.26μg/L的22例患者均发生了MODS,<132.26μg/L的18例患者均未发生MODS;且12例死亡患者HMGB1均≥132.26μg/L.结论 严重创伤患者发生应激性高血糖后即给予胰岛素强化治疗,可有效抑制HMGB1升高,减少MODS发生率;HMGB1可能作为重度创伤患者判断预后的指标.
目的 觀察早期胰島素彊化治療嚴重創傷後血清高遷移率蛋白B1(HMGB1)水平的變化,併探討其與患者預後的關繫.方法 將80例嚴重創傷患者[創傷嚴重度評分(ISS)≥16分]根據最重損傷解剖部位近似原則配對分組.彊化治療組(40例)早期即給予胰島素彊化治療;常規治療組(40例)根據臨床經驗給予常規胰島素治療.記錄患者治療72 h內胰島素用量及血糖水平;于治療後24、36、48、60、72 h檢測血清HMGB1水平;記錄1週內相關終點事件[包括多器官功能障礙綜閤徵(MODS)、死亡];併分析HMGB1水平與預後的關繫.結果 治療72 h內彊化治療組胰島素用量明顯大于常規治療組,血糖水平明顯低于常規治療組.彊化治療組治療36 h時HMGB1水平有所下降,且36、48、60、72 h時HMGB1水平(μg/L)明顯低于常規治療組(36 h:41.3±9.5比52.7±11.5,48 h:48.6±17.6比124.1±22.9,60 h:47.7±23.3比132.9±33.4,72 h:54.3±26.3比140.6±16.5,P<0.05或P<0.01).彊化治療組MODS髮生率和病死率均明顯低于常規治療組(20.0%比55.0%,10.0%比30.0%,均P<0.05).常規治療組內HMGB1≥132.26μg/L的22例患者均髮生瞭MODS,<132.26μg/L的18例患者均未髮生MODS;且12例死亡患者HMGB1均≥132.26μg/L.結論 嚴重創傷患者髮生應激性高血糖後即給予胰島素彊化治療,可有效抑製HMGB1升高,減少MODS髮生率;HMGB1可能作為重度創傷患者判斷預後的指標.
목적 관찰조기이도소강화치료엄중창상후혈청고천이솔단백B1(HMGB1)수평적변화,병탐토기여환자예후적관계.방법 장80례엄중창상환자[창상엄중도평분(ISS)≥16분]근거최중손상해부부위근사원칙배대분조.강화치료조(40례)조기즉급여이도소강화치료;상규치료조(40례)근거림상경험급여상규이도소치료.기록환자치료72 h내이도소용량급혈당수평;우치료후24、36、48、60、72 h검측혈청HMGB1수평;기록1주내상관종점사건[포괄다기관공능장애종합정(MODS)、사망];병분석HMGB1수평여예후적관계.결과 치료72 h내강화치료조이도소용량명현대우상규치료조,혈당수평명현저우상규치료조.강화치료조치료36 h시HMGB1수평유소하강,차36、48、60、72 h시HMGB1수평(μg/L)명현저우상규치료조(36 h:41.3±9.5비52.7±11.5,48 h:48.6±17.6비124.1±22.9,60 h:47.7±23.3비132.9±33.4,72 h:54.3±26.3비140.6±16.5,P<0.05혹P<0.01).강화치료조MODS발생솔화병사솔균명현저우상규치료조(20.0%비55.0%,10.0%비30.0%,균P<0.05).상규치료조내HMGB1≥132.26μg/L적22례환자균발생료MODS,<132.26μg/L적18례환자균미발생MODS;차12례사망환자HMGB1균≥132.26μg/L.결론 엄중창상환자발생응격성고혈당후즉급여이도소강화치료,가유효억제HMGB1승고,감소MODS발생솔;HMGB1가능작위중도창상환자판단예후적지표.
Objective To study the effect of intensive insulin therapy on serum high mobility group box 1(HMGB1)levels and its relationship with the prognosis in early phase of severe trauma. Methods Eighty severe trauma patients[injury severity score(ISS)≥16]were divided into groups according to injury to matched anatomical regions. Forty patients of intensive therapy group were given early intensive insulin therapy, while another 40 patients of the conventional treatment group received routine treatment based on clinical experience with insulin treatment. The insulin dose and the blood glucose levels were recorded within 72 hours after treatment. The relationship between HMGB1 levels and prognosis was analyzed by testing serum HMGB1 levels at 24, 36, 48, 60 or 72 hours after treatment, and clinical terminal events such as multiple organ dysfunction syndrome(MODS)and death rate within 1 week were recorded. Results The insulin dose of intensive therapy group was significantly greater than that of conventional treatment group following the blood glucose levels were significantly lower than those of the conventional treatment group after treatment for 72 hours. The levels of HMGB1(μg/L)lowered after intensive insulin therapy for 36 hours, and were significantly lower than those of conventional treatment group at 36, 48, 60 and 72 hours after intensive treatment(36 hours: 41.3 ± 9.5 vs. 52. 7± 11.5, 48 hours: 48. 6 ± 17. 6 vs. 124. 1 ± 22. 9,60 hours: 47.7±23. 3 vs. 132. 9±33. 4, 72 hours: 54.3±26. 3 vs. 140. 6±16.5, P<0. 05 or P<0. 01).The incidence of MODS and mortality in intensive therapy group was respectively significantly lower than that of the conventional treatment group(20. 0% vs. 55.0%, 10. 0% vs. 30.0%, both P<0. 05). In conventional treatment group the patients with HMGB1≥132.26 μg/L(n=22)occured MODS, and those with HMGB1<132. 26 μg/L(n= 18)did not occur MODS. The HMGB1 levels in death patients(n= 12)were ≥ 132.26 μg/L. Conclusion Early intensive insulin treatment could probably reduce MODS and mortality by inhibiting stress hyperglycemia and serum HMGB1 levels effectively. Serum HMGB1 of severe trauma patients can be used for the clinical indicator of prognosis.