Russell James A, Walley Keith R, Gordon Anthony C, Cooper D James, Hébert Paul C, Singer Joel, Holmes Cheryl L, Mehta Sangeeta, Granton John T, Storms Michelle M, Cook Deborah J, Presneill Jeffrey J
St Paul's Hospital, iCAPTURE Centre, Canada.
Crit Care Med. 2009 Mar;37(3):811-8. doi: 10.1097/CCM.0b013e3181961ace.
Vasopressin and corticosteroids are often added to support cardiovascular dysfunction in patients who have septic shock that is nonresponsive to fluid resuscitation and norepinephrine infusion. However, it is unknown whether vasopressin treatment interacts with corticosteroid treatment.
Post hoc substudy of a multicenter randomized blinded controlled trial of vasopressin vs. norepinephrine in septic shock.
Twenty-seven Intensive Care Units in Canada, Australia, and the United States.
: Seven hundred and seventy-nine patients who had septic shock and were ongoing hypotension requiring at least 5 microg/min of norepinephrine infusion for 6 hours.
Patients were randomized to blinded vasopressin (0.01-0.03 units/min) or norepinephrine (5-15 microg/min) infusion added to open-label vasopressors. Corticosteroids were given according to clinical judgment at any time in the 28-day postrandomization period.
The primary end point was 28-day mortality. We tested for interaction between vasopressin treatment and corticosteroid treatment using logistic regression. Secondary end points were organ dysfunction, use of open-label vasopressors and vasopressin levels.
There was a statistically significant interaction between vasopressin infusion and corticosteroid treatment (p = 0.008). In patients who had septic shock and were also treated with corticosteroids, vasopressin, compared to norepinephrine, was associated with significantly decreased mortality (35.9% vs. 44.7%, respectively, p = 0.03). In contrast, in patients who did not receive corticosteroids, vasopressin was associated with increased mortality compared with norepinephrine (33.7% vs. 21.3%, respectively, p = 0.06). In patients who received vasopressin infusion, use of corticosteroids significantly increased plasma vasopressin levels by 33% at 6 hours (p = 0.006) to 67% at 24 hours (p = 0.025) compared with patients who did not receive corticosteroids.
There is a statistically significant interaction between vasopressin and corticosteroids. The combination of low-dose vasopressin and corticosteroids was associated with decreased mortality and organ dysfunction compared with norepinephrine and corticosteroids.
对于液体复苏和去甲肾上腺素输注无效的感染性休克患者，血管加压素和皮质类固醇常被加用，以支持心血管功能障碍。然而，血管加压素治疗与皮质类固醇治疗之间是否存在相互作用尚不清楚。
一项关于血管加压素与去甲肾上腺素治疗感染性休克的多中心随机双盲对照试验的事后亚组研究。
加拿大、澳大利亚和美国的27个重症监护病房。
779例感染性休克且持续低血压的患者，需要至少以5微克/分钟的速度输注去甲肾上腺素6小时。
患者被随机分为接受盲法血管加压素（0.01 - 0.03单位/分钟）或去甲肾上腺素（5 - 15微克/分钟）输注，并加用开放标签的血管升压药。在随机分组后的28天内，根据临床判断随时给予皮质类固醇。
主要终点为28天死亡率。我们使用逻辑回归分析血管加压素治疗与皮质类固醇治疗之间的相互作用。次要终点包括器官功能障碍、开放标签血管升压药的使用情况以及血管加压素水平。
血管加压素输注与皮质类固醇治疗之间存在统计学显著的相互作用（p = 0.008）。在感染性休克且接受皮质类固醇治疗的患者中，与去甲肾上腺素相比，血管加压素与死亡率显著降低相关（分别为35.9%和44.7%，p = 0.03）。相反，在未接受皮质类固醇治疗的患者中，与去甲肾上腺素相比，血管加压素与死亡率升高相关（分别为33.7%和21.3%，p = 0.06）。在接受血管加压素输注的患者中，与未接受皮质类固醇治疗的患者相比，使用皮质类固醇在6小时时可使血浆血管加压素水平显著升高33%（p = 0.006），在24小时时升高67%（p = 0.025）。
血管加压素与皮质类固醇之间存在统计学显著的相互作用。与去甲肾上腺素和皮质类固醇相比，低剂量血管加压素与皮质类固醇联合使用与死亡率降低和器官功能障碍减少相关。
