Methylene blue: “Magic bullet” for refractory septic shock?

doi:10.3877/cma.j.issn.2096-1537.2024.02.007

Abstract

Abstract:

The optimal start-up timing and reasonable combination of vasoactive drugs has recently been hot spots in the research field of septic shock. The latest Surviving Sepsis Campaign strongly recommend norepinephrine (NE) as first-line agent over other vasopressors. However, NE-related side effects such as immunosuppression and arrhythmia have gotten more and more attentions. High dose of NE has been demonstrated to be independent risk factors associated with mortality of septic shock. Many multicenter, randomized controlled studies have shown that the combination of non-catecholamine vasopressors significantly spared the usage of NE, enhanced blood pressure, and might improve survival outcome. Methylene blue (MB), which has unique mechanism to raise pressure, has often been used as “magic bullet” for refractory vasoplegia shock. But the effectiveness of MB was confined to small sample studies and case reports. MB has promising clinical value due to its low-cost and easy-access even in grassroots hospitals. This review summarizes the combination regimen of non-catecholamines vasopressors in septic shock, and the mechanism, status and prospect of MB, in order to promote agreements on indication, timing, dose and duration of MB administration.

Key words: Methylene blue, Septic shock, Norepinephrine, Non-catecholamine drugs

Li Li, Lina Zhang, Zhaoxin Qian. Methylene blue: “Magic bullet” for refractory septic shock?[J]. Chinese Journal of Critical Care & Intensive Care Medicine(Electronic Edition), 2024, 10(02): 136-142.

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References 55

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纳入研究作者，发表年份	纳入文献的研究例数	纳入标准	亚甲蓝使用方法	ICU住院病死率（%）	主要观察终点	次要观察终点	不良反应
观察性研究
Preiser等^［38］，1995	14	脓毒症休克，充分液体复苏后泵入2种以上升压药物	2 mg/kg推注；6例90 min后再次推注2 mg/kg	78.6	90 min后MAP、外周血管阻力、左室做功显著增加	肺动脉压、肺毛细血管楔压、心率、CI、氧供、氧耗无明显改变。90 min后乳酸明显下降	皮肤、尿液变蓝
Daemen-Gubbles等^［39］，1995	9	脓毒症休克，充分液体复苏后泵入2种以上升压药物	2 mg/kg推注	88.9	30 min后MAP和CI明显增加，2 h后恢复至基线水平	氧供、氧摄取、动脉顺应性明显增加；外周血管阻力有增加趋势	乳酸、环磷酸鸟苷、高铁血红蛋白无明显改变
Gachot等^［40］，1995	6	严重脓毒症休克，NE 0.07 μg/（kg·min），Epi 0.03 μg/（kg·min）	3 mg/kg推注	83.3	MAP和外周血管阻力、肺动脉压和肺毛细血管楔压明显增加；2~3 h后恢复至基线水平	CI、氧供、心率、右房压、乳酸没有改变	氧合指数显著下降
Andresen等^［41］，1998	10	脓毒症休克，同时应用2种以上升压药物[NE>0.2 μg/（kg·min），Epi>0.1 μg/（kg·min），Dopa>5 μg/（kg•min）]	1 mg/kg推注	80.0	MAP、外周血管阻力、肺动脉压明显增加	心率、毛细血管楔压、CI、肺血管阻力、氧供、氧耗不变；氧合指数未改变；乳酸下降，但差异无统计学意义	/
Weingartner等^［42］，1999	10	顽固性脓毒症休克	4 mg/kg推注	90.0	MAP和外周血管阻力明显增加；40、60 min时左室做功指数明显增加	60 min混合静脉血氧饱和度下降，乳酸显著下降；心率、肺毛细血管楔压、CI、氧供、氧耗未改变	20 min肺血管阻力增加；40 min氧合指数下降
Donati等^［43］，2002	15	脓毒症休克，充分液体复苏后NE或Dopa>1.5~3 μg/（kg·min）泵入	3 mg/kg推注	60.0	MAP显著增加，2 h后恢复至基线水平	肺动脉压显著增加，CI和肺动脉楔压不变，左室做功指数增加	血浆渗透压轻微增加
Park等^［44］，2005	20	脓毒症休克，充分液体复苏后NE>0.1 μg/（kg·min）或Dopa>20 μg/（kg·min）泵入	1 mg/kg推注	65.0	MAP、外周血管阻力、肺动脉压明显增加	心率、毛细血管楔压、CI、肺血管阻力、氧供、氧耗不变	NO、IL-1、IL-10、TNF-α水平无改变
随机对照研究
Kirov等^［45］，2001	亚甲蓝vs 0.9%NaCl溶液：10 vs 10	顽固性脓毒症休克	2 mg/kg推注，2 h后0.25、0.5、1、2 mg/kg各维持1 h	50.0 vs 70.0^*	实验组MAP增加，NE、Epi和Dopa的需求分别下降87%、81%和40%	实验组氧供未变，对照组氧供下降；器官功能改变无组间差异；实验组体温、NO代谢物下降	尿液蓝色2~4 d，皮肤蓝色1~3 d
Memis等^［46］，2002	亚甲蓝vs 0.9%NaCl溶液：15 vs 15	脓毒症1.0定义和至少一个器官功能损害表现	0.5 mg/（kg•h）维持6 h	26.6 vs 26.6	用药后即刻MAP增加，24 h和48 h无差别	细胞因子水平无差异	尿液蓝色；高铁血红蛋白血症24 h后缓解
Juffermans等^［47］，2010	不同剂量亚甲蓝，4 vs 6 vs 5	脓毒症休克	1 mg/kg vs 3 mg/kg vs 7 mg/kg推注	75.0 vs 50.0 vs 60.0^*	MAP、外周血管阻力、肺动脉压、肺毛细血管楔压、中心静脉压、心率、CI、左室做功指数一过性增加	MAP、肺动脉压、肺毛细血管楔压、CI、左室做功指数的增加呈剂量相关性。肺血管阻力指数未改变	7 mg/kg组动脉氧分压明显下降；胃-动脉二氧化碳分压差明显增加，且呈剂量相关性
熊响清等^［48］，2010	亚甲蓝vs NE：20 vs 20	脓毒症休克患者急诊术中	亚甲蓝 vs NE：0.5~1.0 mg/（kg·h）vs 0.5~2 μg/（kg·min）	/	亚甲蓝组30、60、90 min时MAP显著高于NE组	亚甲蓝组各时间段氧供、氧耗高于NE组，乳酸低于NE组	/
陆雅萍等^［49］，2019	亚甲蓝单次vs维持泵入vs 0.9%NaCl溶液：18 vs 18 vs 18	脓毒症休克，MAP<65 mmHg且血乳酸>2 mmol/L	2 mg/kg单次推注 vs 2 mg/kg推注后，2 mg/kg维持24 h泵入 vs 等量0.9% NaCl溶液	16.7 vs 11.2 vs 27.8^*	两实验组用药24 h后NE用量明显降低，NE总量减少	持续用药组第1~5 d灌注指数优于单次用药及对照组，氧合指数无组间差异	/

纳入研究作者，发表年份	纳入文献的研究例数	纳入标准	亚甲蓝使用方法	ICU住院病死率（%）	主要观察终点	次要观察终点	不良反应
观察性研究
Preiser等^［38］，1995	14	脓毒症休克，充分液体复苏后泵入2种以上升压药物	2 mg/kg推注；6例90 min后再次推注2 mg/kg	78.6	90 min后MAP、外周血管阻力、左室做功显著增加	肺动脉压、肺毛细血管楔压、心率、CI、氧供、氧耗无明显改变。90 min后乳酸明显下降	皮肤、尿液变蓝
Daemen-Gubbles等^［39］，1995	9	脓毒症休克，充分液体复苏后泵入2种以上升压药物	2 mg/kg推注	88.9	30 min后MAP和CI明显增加，2 h后恢复至基线水平	氧供、氧摄取、动脉顺应性明显增加；外周血管阻力有增加趋势	乳酸、环磷酸鸟苷、高铁血红蛋白无明显改变
Gachot等^［40］，1995	6	严重脓毒症休克，NE 0.07 μg/（kg·min），Epi 0.03 μg/（kg·min）	3 mg/kg推注	83.3	MAP和外周血管阻力、肺动脉压和肺毛细血管楔压明显增加；2~3 h后恢复至基线水平	CI、氧供、心率、右房压、乳酸没有改变	氧合指数显著下降
Andresen等^［41］，1998	10	脓毒症休克，同时应用2种以上升压药物[NE>0.2 μg/（kg·min），Epi>0.1 μg/（kg·min），Dopa>5 μg/（kg•min）]	1 mg/kg推注	80.0	MAP、外周血管阻力、肺动脉压明显增加	心率、毛细血管楔压、CI、肺血管阻力、氧供、氧耗不变；氧合指数未改变；乳酸下降，但差异无统计学意义	/
Weingartner等^［42］，1999	10	顽固性脓毒症休克	4 mg/kg推注	90.0	MAP和外周血管阻力明显增加；40、60 min时左室做功指数明显增加	60 min混合静脉血氧饱和度下降，乳酸显著下降；心率、肺毛细血管楔压、CI、氧供、氧耗未改变	20 min肺血管阻力增加；40 min氧合指数下降
Donati等^［43］，2002	15	脓毒症休克，充分液体复苏后NE或Dopa>1.5~3 μg/（kg·min）泵入	3 mg/kg推注	60.0	MAP显著增加，2 h后恢复至基线水平	肺动脉压显著增加，CI和肺动脉楔压不变，左室做功指数增加	血浆渗透压轻微增加
Park等^［44］，2005	20	脓毒症休克，充分液体复苏后NE>0.1 μg/（kg·min）或Dopa>20 μg/（kg·min）泵入	1 mg/kg推注	65.0	MAP、外周血管阻力、肺动脉压明显增加	心率、毛细血管楔压、CI、肺血管阻力、氧供、氧耗不变	NO、IL-1、IL-10、TNF-α水平无改变
随机对照研究
Kirov等^［45］，2001	亚甲蓝vs 0.9%NaCl溶液：10 vs 10	顽固性脓毒症休克	2 mg/kg推注，2 h后0.25、0.5、1、2 mg/kg各维持1 h	50.0 vs 70.0^*	实验组MAP增加，NE、Epi和Dopa的需求分别下降87%、81%和40%	实验组氧供未变，对照组氧供下降；器官功能改变无组间差异；实验组体温、NO代谢物下降	尿液蓝色2~4 d，皮肤蓝色1~3 d
Memis等^［46］，2002	亚甲蓝vs 0.9%NaCl溶液：15 vs 15	脓毒症1.0定义和至少一个器官功能损害表现	0.5 mg/（kg•h）维持6 h	26.6 vs 26.6	用药后即刻MAP增加，24 h和48 h无差别	细胞因子水平无差异	尿液蓝色；高铁血红蛋白血症24 h后缓解
Juffermans等^［47］，2010	不同剂量亚甲蓝，4 vs 6 vs 5	脓毒症休克	1 mg/kg vs 3 mg/kg vs 7 mg/kg推注	75.0 vs 50.0 vs 60.0^*	MAP、外周血管阻力、肺动脉压、肺毛细血管楔压、中心静脉压、心率、CI、左室做功指数一过性增加	MAP、肺动脉压、肺毛细血管楔压、CI、左室做功指数的增加呈剂量相关性。肺血管阻力指数未改变	7 mg/kg组动脉氧分压明显下降；胃-动脉二氧化碳分压差明显增加，且呈剂量相关性
熊响清等^［48］，2010	亚甲蓝vs NE：20 vs 20	脓毒症休克患者急诊术中	亚甲蓝 vs NE：0.5~1.0 mg/（kg·h）vs 0.5~2 μg/（kg·min）	/	亚甲蓝组30、60、90 min时MAP显著高于NE组	亚甲蓝组各时间段氧供、氧耗高于NE组，乳酸低于NE组	/
陆雅萍等^［49］，2019	亚甲蓝单次vs维持泵入vs 0.9%NaCl溶液：18 vs 18 vs 18	脓毒症休克，MAP<65 mmHg且血乳酸>2 mmol/L	2 mg/kg单次推注 vs 2 mg/kg推注后，2 mg/kg维持24 h泵入 vs 等量0.9% NaCl溶液	16.7 vs 11.2 vs 27.8^*	两实验组用药24 h后NE用量明显降低，NE总量减少	持续用药组第1~5 d灌注指数优于单次用药及对照组，氧合指数无组间差异	/

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