口服磷酸钠后,细胞钾耗竭易发生低钾血症。

A G Hill, W Teo, A Still, B R Parry, L D Plank, G L Hill
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引用次数: 2

摘要

背景:口服磷酸钠已成为一种有吸引力的替代聚乙二醇用于结肠清洁准备择期结肠手术。然而,它的使用与低血钾有关。本研究的作者验证了一种假设,即口服磷酸钠肠制剂的细胞钾耗损患者有低钾血症的显著风险。方法:23例患者在口服磷酸钠肠道准备前,采用全身计数法测定全身钾含量,生物阻抗法测定细胞内水量。将患者分为血清钾降至3.5 mmol/L及以下组(1组)和未降至3.5 mmol/L组(2组)。结果:口服磷酸钠期间血清钾浓度下降与给药前细胞内钾浓度呈显著负相关(r = -0.65, P = 0.0009)。在第1组中,血清钾浓度从4.1+/-0.1(平均标准误差(SEM)) mmol/L下降到3.2+/-0.1 mmol/L (P < 0.0001),而在第2组中,由于磷酸钠处理,该浓度没有显著变化(4.0+/-0.1 vs 3.9+/-0.1 mmol/L)。第1组给予磷酸钠前细胞内钾浓度显著降低(117+/-9 mmol/L vs 143+/-7 mmol/L, P < 0.05)。结论:口服磷酸钠治疗被认为细胞钾缺乏的患者时应谨慎。这些患者在这种治疗后有低钾血症的危险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cellular potassium depletion predisposes to hypokalaemia after oral sodium phosphate.

Background: Oral sodium phosphate has become an attractive alternative to polyethylene glycol for colonic cleansing preparatory to elective colorectal surgery. Its use, however, has been associated with hypokalaemia. The authors of the present study tested the hypothesis that patients with cellular depletion of potassium are at significant risk for hypokalaemia with oral sodium phosphate bowel preparation.

Methods: In 23 patients, total body potassium was measured by whole-body counting and intracellular water volume was measured by bioimpedance analysis before oral sodium phosphate bowel preparation. Patients were divided into those whose serum potassium fell to 3.5 mmol/L or lower (Group 1) and those whose did not after sodium phosphate treatment (Group 2).

Results: The fall in serum potassium concentration over the period of oral sodium phosphate administration was significantly negatively correlated with intracellular potassium concentration measured prior to administration (r = -0.65, P = 0.0009). In Group 1, serum potassium concentration fell from 4.1+/-0.1 (standard error of the mean (SEM)) mmol/L to 3.2+/-0.1 mmol/L (P < 0.0001) while in Group 2 there was no significant change in this concentration (4.0+/-0.1 vs 3.9+/-0.1 mmol/L) as a result of sodium phosphate treatment. Intracellular potassium concentration prior to administration of sodium phosphate was significantly lower in Group 1 (117+/-9 mmol/L vs 143+/-7 mmol/L, P < 0.05).

Conclusions: Caution should be exercised when treating patients with oral sodium phosphate who are considered to be cellularly depleted of potassium. These patients are at risk of hypokalaemia after this treatment.

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