Hamill-Ruth R J, McGory R
Department of Anesthesiology, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
Crit Care Med. 1996 Jan;24(1):38-45. doi: 10.1097/00003246-199601000-00009.
The aims of this study were to evaluate the safety and efficacy of magnesium replacement therapy and to determine its effect on potassium retention in hypokalemic, critically ill patients.
A prospective, double-blind, randomized, placebo-controlled trial.
A surgical intensive care unit (ICU).
A total of 32 adult surgical ICU patients were admitted to the study on the basis of documented hypokalemia (potassium of < 3.5 mmol/L) within the 24-hr period before entering the study. Patients were randomized to receive either placebo (n = 15) or magnesium sulfate (n = 17). One patient from each group was excluded from the study due to failure to complete the full series of doses.
Patients received a "test dose" of either magnesium sulfate (2 g, 8 mmol) or placebo (5% dextrose in water) infused over 30 mins every 6 hrs for eight doses. The next schedule test dose was held if hypermagnesemia (magnesium of > 2.8 mg/dL [> 1.15 mmol/L]) was documented at any time during the study. Routine replacements of potassium and magnesium continued during the duration of the study, when clinically indicated, for serum potassium concentrations of 3.5 mmol/L or serum magnesium concentrations of < 1.8 mg/dL (< 0.74 mmol/L).
Age, weight, and Acute Physiology and Chronic Health Evaluation II scores were recorded on entry into the study. Just before administration of each test dose, blood was drawn for magnesium and potassium, bicarbonate, pH, and glucose determinations, and an aliquot of the preceding 6 hrs urine collection was sent for magnesium and potassium determinations. Serum calcium, phosphate, urea nitrogen, and creatinine concentrations were measured daily. The amounts of magnesium and potassium administered via parenteral nutrition, tube feeding, and replacement infusions were calculated for each 6-hr interval. The amounts of magnesium and potassium excreted in the urine were similarly assessed. The groups showed no differences with regard to age, weight, Acute Physiology and Chronic Health Evaluation II scores, or initial serum magnesium concentration. Initial potassium, bicarbonate, pH, calcium, phosphate, glucose, blood urea nitrogen, and creatinine values were not different between groups. Patients receiving magnesium sulfate showed a statistically significant increase in serum magnesium concentration at 6 hrs when compared with placebo, as well as with itself at time 0 (p < .0001), a difference maintained throughout the study. Compared with the placebo group, the total amount of elemental magnesium administered was significantly greater in the treatment group (1603 +/- 124 vs. 752 +/- 215 mg [65.7 +/- 5.8 vs. 30.8 +/- 8.8 mmol], p < .0001), as was urine magnesium excretion (1000 +/- 156 vs. 541 +/- 68 mg [41.0 +/- 6.4 vs. 22.2 +/- 2.8 mmol] p < .0001). However, the net magnesium balance (total magnesium in - total urine magnesium) was significantly more positive in the treatment group (612 +/- 180 vs. 216 +/- 217 mg [25.1 +/- 7.4 vs. 8.9 +/- 8.9 mmol], p < .005). The treatment and control groups had the same serum potassium concentrations and did not receive different amounts of potassium (245 +/- 39 vs. 344 +/- 45 mmol, respectively, p = .06), although the treatment group required less potassium replacement/6 hrs by 30 hrs compared with itself at time 0 (p < .05). Despite the same serum potassium values, the net potassium balance for 48 hrs was positive in the treatment group (+ 72 +/- 32 mmol) and negative in the control group (-74 +/- 95 mmol, p < .05). There were no complications associated with the magnesium sulfate administration.
Magnesium sulfate administered according to the above regimen safety and significantly increases the circulating magnesium concentration. Despite greater urine magnesium losses in the treatment group, this group exhibited significantly better magnesium retention.
本研究旨在评估镁补充疗法的安全性和有效性,并确定其对低钾血症重症患者钾潴留的影响。
一项前瞻性、双盲、随机、安慰剂对照试验。
外科重症监护病房(ICU)。
共有32名成年外科ICU患者在进入研究前24小时内根据记录的低钾血症(血钾<3.5 mmol/L)入选本研究。患者被随机分为接受安慰剂组(n = 15)或硫酸镁组(n = 17)。每组各有1名患者因未完成全部剂量而被排除在研究之外。
患者每6小时接受一次“试验剂量”的硫酸镁(2 g,8 mmol)或安慰剂(5%葡萄糖水溶液),30分钟内输注完毕,共八剂。如果在研究期间任何时间记录到高镁血症(血镁>2.8 mg/dL [>1.15 mmol/L]),则暂停下一次计划的试验剂量。在研究期间,当临床指征显示血清钾浓度为3.5 mmol/L或血清镁浓度<1.8 mg/dL(<0.74 mmol/L)时,继续常规补充钾和镁。
研究开始时记录年龄、体重和急性生理与慢性健康状况评分II(APACHE II)。每次试验剂量给药前,采集血液测定镁、钾、碳酸氢根、pH值和葡萄糖,并将前6小时收集的尿液样本送去测定镁和钾。每天测量血清钙、磷、尿素氮和肌酐浓度。计算每6小时间隔通过肠外营养、管饲和补充输注给予的镁和钾的量。同样评估尿中排出的镁和钾的量。两组在年龄、体重、APACHE II评分或初始血清镁浓度方面无差异。两组的初始钾离子、碳酸氢根、pH值、钙离子、磷离子、葡萄糖、血尿素氮和肌酐值无差异。与安慰剂组相比,接受硫酸镁治疗的患者在6小时时血清镁浓度有统计学显著升高,与0小时时相比也有升高(p < 0.0001),整个研究期间差异持续存在。与安慰剂组相比,治疗组给予的元素镁总量显著更多(1603±124 vs. 752±215 mg [65.7±5.8 vs. 30.8±8.8 mmol],p < 0.0001),尿镁排泄量也更多(1000±156 vs. 541±68 mg [41.0±6.4 vs. 22.2±2.8 mmol],p < 0.0001)。然而,治疗组的净镁平衡(摄入的总镁量 - 尿中总镁量)显著更正向(612±180 vs. 216±217 mg [25.1±7.4 vs. 8.9±8.9 mmol],p < 0.005)。治疗组和对照组的血清钾浓度相同,且接受的钾量无差异(分别为245±39 vs. 344±45 mmol,p = 0.06),尽管治疗组与0小时时相比,在30小时时每6小时所需的钾补充量减少(p < 0.05)。尽管血清钾值相同,但治疗组48小时的净钾平衡为正值(+72±32 mmol),而对照组为负值(-74±95 mmol,p < 0.05)。硫酸镁给药未出现并发症。
按照上述方案给予硫酸镁安全且显著提高循环镁浓度。尽管治疗组尿镁丢失更多,但该组的镁潴留明显更好。