背景:最近的报道表明,在使用高渗NaCl治疗的蛛网膜下腔出血(SAH)患者中,高氯血症与急性肾损伤(AKI)的发生有关。我们报告了一项试验,比较了两种不同氯化物含量的高渗溶液对SAH患者血清氯化物浓度的影响,主要结果旨在限制氯化物升高。
方法:一项针对脑水肿的低氯气高渗溶液(ACETatE)试验是一项单中心试验,双盲,双假人,比较23.4%NaCl和16.4%NaCl/醋酸钠推注治疗SAH患者脑水肿的随机先导试验。当患者出现高氯血症(血清Cl-≥109mmol/L)并需要高渗治疗时,就进行了随机化。
结果:我们招募了59名患者,其中32人发展为高氯血症,需要高渗治疗。15例患者随机分为23.4%NaCl组,17例患者随机分为16.4%NaCl/乙酸钠组。尽管两组的血清氯化物水平相似地增加,在研究期结束时,NaCl/醋酸盐组的Cl-负荷显着降低(978mEqvs.2,464mEq,p<0.01)。次要结果分析显示,乙酸钠组的AKI发生率降低(NaCl组的AKI发生率为53.3%乙酸钠组11.8%,p=0.01)。两种溶液对ICP还原有相似的影响,但NaCl/醋酸盐处理对输注后立即Na+浓度有更显著的影响(增加2.2±2.8vs.1.4±2.6,(p<0.01))。两组间近端肾小管肾生物标志物的浓度不同。
结论:我们的初步试验表明,用16.4%NaCl/乙酸钠输注代替23.4%NaCl输注治疗SAH患者脑水肿的可行性和安全性。两组的高氯血症程度相似。与23.4%NaCl输注相比,16.4%NaCl/乙酸钠输注导致较低的Cl-负荷和AKI率。需要进一步的多中心研究来证实这些结果。
背景:clinicaltrials.gov#NCT03204955,于2017年6月28日注册。
BACKGROUND: Recent reports have demonstrated that among patients with subarachnoid hemorrhage (SAH) treated with hypertonic NaCl, resultant hyperchloremia has been associated with the development of acute kidney injury (AKI). We report a
trial comparing the effect of two hypertonic solutions with different chloride contents on the resultant serum chloride concentrations in SAH patients, with a primary outcome aimed at limiting chloride elevation.
METHODS: A low ChloridE hyperTonic solution for brain Edema (ACETatE)
trial is a single-center, double-blinded, double-dummy, randomized pilot
trial comparing bolus infusions of 23.4% NaCl and 16.4% NaCl/Na-acetate for the treatment of cerebral edema in patients with SAH. Randomization occurred when patients developed hyperchloremia (serum Cl- ≥ 109 mmol/L) and required hyperosmolar treatment.
RESULTS: We enrolled 59 patients, of which 32 developed hyperchloremia and required hyperosmolar treatment. 15 patients were randomized to the 23.4% NaCl group, and 17 patients were randomized to the 16.4% NaCl/Na-acetate group. Although serum chloride levels increased similarly in both groups, the NaCl/Acetate group showed a significantly lower Cl- load at the end of the
study period (978mEq vs. 2,464mEq, p < 0.01). Secondary outcome analysis revealed a reduced rate of AKI in the Na-acetate group (53.3% in the NaCl group vs. 11.8% in the Na-acetate group, p = 0.01). Both solutions had similar effects on ICP reduction, but NaCl/Acetate treatment had a more prominent effect on immediate post-infusion Na+ concentrations (increase of 2.2 ± 2.8 vs. 1.4 ± 2.6, (p < 0.01)). Proximal tubule renal biomarkers differed in concentration between the two groups.
CONCLUSIONS: Our pilot trial showed the feasibility and safety of replacing 23.4% NaCl infusions with 16.4% NaCl/Na-acetate infusions to treat cerebral edema in patients with SAH. The degree of
hyperchloremia was similar in the two groups. 16.4% NaCl/Na-acetate infusions led to lower Cl- load and AKI rates than 23.4% NaCl infusions. Further multi-center studies are needed to corroborate these results.
BACKGROUND: clinicaltrials.gov # NCT03204955, registered on 6/28/2017.